UBC Theses and Dissertations

UBC Theses Logo

UBC Theses and Dissertations

The comorbidity of early childhood caries and iron deficiency in preschool children Szeto, Ann 2004

Your browser doesn't seem to have a PDF viewer, please download the PDF to view this item.

Item Metadata


831-ubc_2004-0651.pdf [ 5.37MB ]
JSON: 831-1.0092878.json
JSON-LD: 831-1.0092878-ld.json
RDF/XML (Pretty): 831-1.0092878-rdf.xml
RDF/JSON: 831-1.0092878-rdf.json
Turtle: 831-1.0092878-turtle.txt
N-Triples: 831-1.0092878-rdf-ntriples.txt
Original Record: 831-1.0092878-source.json
Full Text

Full Text

The Comorbidity of  Early Childhood Caries and Iron Deficiency In Preschool Children By Ann C. Y. Szeto B.A., The University of  British Columbia, 1997 Dip.DH, Vancouver Community College, 2000 A Thesis Submitted in Partial Fulfillment  of ( The Requirements for  the Degree of Master of  Science in The Faculty of  Graduate Studies (Department of  Oral Health Sciences) We accept this thesis as conforming To the required standards The University of  British Columbia October 2004 © Ann C. Y. Szeto The Comorbidity of Early Childhood Caries and Iron Deficiency in Preschool Children by Ann C.Y. Szeto B.A., The University of British Columbia, 1997 Dip.DH, Vancouver Community College, 2000 A Thesis Submitted in Partial Fulfillment of the Requirements for the Degree of Master of Science in The Faculty of Dentistry (Department of Oral Health Sciences) Supervised by Dr. Rosamund L. Harrison We accept this thesis as conforming to the required standards The University of British Columbia October 2004 © Ann C.Y. Szeto THE UNIVERSITY OF BRITISH COLUMBIA FACULTY OF GRADUATE STUDIES Library Authorization LJ In presenting this thesis in partial fulfillment  of the requirements for an advanced degree at the University of British Columbia, I agree that the Library shall make it freely available for reference and study. I further  agree that permission for extensive copying of this thesis for scholarly purposes may be granted by the head of my department or by his or her representatives. It is understood that copying or publication of this thesis for financial gain shall not be allowed without my written permission. Pino CM.  SzeJHo OS  / 1 0 / 2 0 0 4 Name of Author (please  print) Date (dd/mm/yyyy) Title of Thesis: T W e C o c w o r U c U h ^ o£~ GcaxU^ CgtvveS. g t ^ c i I \ e R c l m c . ^ vn C V I T U W ^ ; . Degree: (YWxste^ pip S r A i ^ n Year: 2 0 0 4 Department of Occk.I  - H e g i W n Sd&nc^S. The University of British Columbia Vancouver, BC Canada grad.ubc.ca/forms/?formlD=THS page 1 of 1 last  updated:  17-Sep-04 TABLE OF CONTENTS List of  Tables vii List of  Figures viii Acknowledgements ix Dedication xi 1. INTRODUCTION 1 1.1. Purpose of  Study 3 2. REVIEW OF THE LITERATURE 4 2.1. Early Childhood Caries 4 2.1.1. Definition  4 2.1.2. Prevalence 5 2.1.3. Biological Risk Factors 6 Microflora  6 Host 8 Saliva 8 Tooth maturation or defects  9 Substrate 10 Cariogenicity 10 2.1.4. Non-Biological Risk Factors 13 Socioeconomic Status 13 Parenting and Family Issues 14 Preventive Dentistry 15 Dental homecare 15 Access to Fluoride 16 2.1.5. Implications for  Child Health 17 2.2. Dietary Iron 19 2.2.1. Requirements (for  Children) 20 2.2.2. Bioavailability and Absorption 21 2.2.3. Iron Deficiency  23 Prevalence 23 Stages 24 Iron depletion 25 Iron deficiency  erythropoiesis (IDE) 25 Iron deficiency  anemia (IDA) 26 Risk Factors 27 Child's age 27 Socioeconomic status 28 Health conditions 29 Child's feeding  practices 30 Implications for  Child Health 31 Cognitive concerns 31 Physical concerns 32 2.3. Commonality between ECC and ID 34 3. METHODS 35 3.1. Overview of  Study 35 3.1.1. Planning the Study 35 3.1.2. Stage 1: Recruitment 36 3.1.3. Stage 2: Dental and Nutrition Clinics 37 3.2. Clinical Protocol 38 3.2.1. Questionnaires 38 Screening Questionnaire 38 Food Frequency Questionnaire 38 Oral Care Questionnaire 39 3.2.2. Clinical Assessments 39 Anthropometrics 39 Dental Examination 39 Blood Work Assessments 40 3.2.3. Data Analysis 40 4. RESULTS 43 4.1. Stage 1 Data: Screening Questionnaire (SQ) 43 4.1.1. Demographics 43 4.1.2. Eating Patterns 45 4.2. Stage 2 Data: Dental and Nutrition Clinics 46 4.2.1. Anthropometrics 46 4.2.2. Eating Patterns from  Food Frequency Questionnaire 47 4.2.3. Dental Health 49 4.2.4. Caries Status 50 4.3. Explanatory Variables and Caries Status 51 4.3.1. All children 51 4.3.2. Children Under 36 Months 54 4.3.3. Children Over 36 Months 55 4.4. Iron Store Status 57 4.5. Explanatory Variables for  ID 58 4.5.1. All Children 59 4.5.2. Children Under 36 Months 61 4.5.3. Children Over 36 Months 62 5. DISCUSSION 63 5.1. Limitations of  the Study 63 5.1.1. Sampling Method and Recruitment Strategy 63 5.1.2. Age Range of  Participants 64 5.1.3. Social Desirability Bias 65 5.1.4. Screening Questionnaire 66 5.1.5. Food Frequency Questionnaire 66 5.2. Characteristics of  the Study Sample 68 5.3. Early Childhood Caries (ECC) 71 5.3.1. Definition  and Prevalence 71 5.3.2. Explanatory Variables and Caries 72 5.4. Iron Deficiency  (ID) 77 5.4.1. Prevalence of  Iron Deficiency  77 5.4.2. Explanatory Variables and Iron Deficiency  78 5.5. Early Childhood Caries, Iron Deficiency  and Common Explanatory Variables.... 80 5.6. Conclusion 81 5.7. Recommendations for  Future Research 82 6. REFERENCES 84 7. APPENDICES 98 LIST OF TABLES Table 1 Iron requirements for  children 21 Table 2 Classification  of  iron deficiency  anemia 27 Table 3 Demographics of  study sample 44 Table 4 Eating patterns from  screening questionnaire 46 Table 5 Anthropometric measurements of  study population 47 Table 6 Sugar consumption of  study sample (daily) from  FFQ 48 Table 7 Beverage consumption reporting on the SQ and FFQ 48 Table 8 Dental data from  the oral health questionnaire 49 Table 9 Caries status of  study sample from  the dental questionnaire 51 Table 10 Select variables and caries status for  all children 52 Table 11 Logistic regression of  select variables of  significance  53 Table 12 Sugar consumption for  all children under 36 months 54 Table 13 Select variables of  caries for  children over 36 months 56 Table 14 Iron store status of  study sample from  blood analysis 58 Table 15 Select variables of  iron status for  all children 60 Table 16 Iron stores & milk and total fluid  intake 61 Table 17 Daily milk consumption and iron status for  children under 36 mos.. 62 Table 18 Select studies on iron deficiency  anemia and low iron stores 78 LIST OF FIGURES Figure 1 Stages of  development of  iron deficiency  24 Figure 2 Age distribution 44 Figure 3 Prevalence of  iron deficiency  stages in study sample 58 Acknowledgements I would like to extend my most sincere thanks and gratitude to those who have provided encouragement and support throughout my graduate studies. To Dr. Rosamund Harrison, my graduate supervisor, thank you for  your unfaltering patience and encouragement. Your guidance, continued support, and wisdom have been a source of  inspiration. To Dr. Sheila Innis, my committee member, I am very appreciative of  your encouragement and the many opportunities you have provided for  me to grow as an academic. To Dr. Derkson, my committee member, thank you for  your insights and sharing your experiences with me. To Professor  Bonnie Craig, my committee member, thank you for  believing in me. I am forever  grateful  for  your encouragement in the pursuit of  my studies. To Dr. Pam Glassby, Tana Wyman, and staff  members of  the Vancouver Coastal Health Authority, thank you for  all your support in my research project. Your insight and patience was very much appreciated. To the parents and children who participated in the study, thank you for  your time and patience. To Ziba Vaghri, my fellow  graduate student, thank you for  your support and friendship through the project. To my dear parents whose relentless love, support, and sacrifices  have allowed me to pursue my goals. You both are forever  a cherished source of  inspiration in my life. To my sister May, brother Simon, and their families,  thank you for  your patience and support throughout my studies. Your understanding and encouragement will always be remembered. And to my loving husband Carlos, thank you for  your unconditional love and support through the years. Your understanding and continued encouragement has given me the strength to pursue my goals. Thank you for  always believing in me. Dedicated  to my dear  parents and my loving  husband,  Carlos Chapter 1 1. INTRODUCTION Early childhood is an important stage in a child's life.  Normal growth and development at this stage can be hindered by the common, but preventable, conditions of  early childhood caries (ECC) and iron deficiency  (ID). ECC is a serious condition that affects  thousands of  young B.C. children on an annual basis. Further, dental treatment under general anesthetic (GA) is the most common reason for  a child to be admitted to BC hospitals (Association of  Dental Surgeons of  British Columbia [ADSBC], 2001). A conservative estimate of  the annual cost of  treating ECC under GA in BC exceeds $10.5 million (ADSBC, 2001). In addition to the financial  costs associated with treatment, this preventable condition limits access to operating rooms for  children with other medical conditions (ADSBC, 2001). Iron deficiency  is the most common nutritional deficiency  of  young children. Infants from  6 months to 2 years of  age are especially vulnerable to this condition because by age 4-6 months, the body becomes deplete of  its gestational iron stores and an adequate intake of  iron is essential to prevent the development of  iron deficiency  (Looker, Dallman, Carroll, Gunter, & Johnson, 1997). Meeting iron requirements are further challenged by the onset of  weaning and the rapid physical growth of  infants  and toddlers. In fact,  during early childhood, the recommended intake of  iron relative to body weight exceeds that at any other stage of  life,  including that of  adult men. In addition, children are challenged to receive adequate dietary iron because they tend to consume soft,  plant-based foods  (carbohydrates) which have less available iron than meat which requires more chewing. Further, children also consume smaller quantities of  foods  overall. Therefore,  careful  dietary planning is important to ensure young children meet their high dietary iron requirements. Both ECC and ID can negatively affect  the quality of  life  of  young children. Dental decay can be painful  and diminish a child's ability to eat nutritiously and sleep properly (ADSBC, 2001). Children with ID tend to fatigue  easily and have a decreased appetite. Further, irreversible developmental and cognitive delays are associated with prolonged ID (Michaelsen, Weaver, Branca, & Robertson, 2000). Therefore,  both ECC and ID may have an immense impact on a child's physical growth and social development. ECC and ID are common conditions with complex multifactorial  etiologies. Both conditions are especially prevalent in young children from  lower socioeconomic backgrounds. Moreover, unhealthy dietary and feeding  practices are risk factors common to both ECC and ID. Excessive consumption of  beverages, especially cow's milk, may increase a child's risk to both conditions. Fortunately, both ECC and ID are preventable. Establishing that there is a dietary link between the two conditions may bring increased commitment to prevention of  both conditions from  all healthcare providers who work with young children and their families.  Such an intersectoral approach to preventing both these conditions may eventually result in a decreased prevalence of  both ECC and ID in high risk children. 1.1. Purpose of  Study The overall goal of  this study was to explore the dietary risk factors  that may contribute to both ECC and ID. The objectives of  the study were to: 1. determine the prevalence of  dental decay and iron deficiency  in a sample of preschool children from  Vancouver, British Columbia, 2. explore the socio-demographic variables, dietary habits and dental health practices that may be associated with early childhood caries and iron deficiency  in these children, and 3. explore a possible relationship between early childhood caries and iron deficiency by investigating common explanatory variables, most specifically  dietary patterns. Chapter 2 2. REVIEW OF THE LITERATURE 2.1. Early Childhood Caries. 2.1.1. Definition Dental caries in young children is a serious problem. Early childhood caries (ECC) is the term currently used to refer  to extensive decay in young children. In the past, the term "nursing bottle mouth" was used to describe a pattern of  decay affecting  the primary maxillary anterior teeth and the maxillary and mandibular first  molars (Fass, 1962). Other terms including nursing bottle caries, nursing bottle syndrome, milk bottle syndrome, baby bottle caries, and baby bottle tooth decay have also been used (Ripa, 1998). All these terms reflect  the understanding of  the day that this characteristic pattern of  decay was purely a result of  inappropriate baby bottle use. In 1994, a conference  at the Center for  Disease Control and Prevention developed the currently used term, "early childhood caries" (Center for  Disease Control and Prevention [CDCP], 1994). This new terminology represents an evolving understanding of  the multifactorial  etiology of  ECC (Reisine & Douglass, 1998) and the current awareness that the relationship between bottle habits and rampant tooth decay is not absolute (Tinanoff,  1998). In other words, not all children with ECC have a history of  inappropriate bottle use, and conversely, many children with negative bottle feeding  habits do not develop ECC. In 2003, the American Academy of  Pediatric Dentistry published their definition  of ECC. The condition was defined  as the presence of  one or more decayed (cavitated or noncavitated), missing (due to decay) or filled  tooth surface  (dmfs)  on any primary tooth in a child less than 6 years of  age. Severe ECC (S-ECC) was the presence of  caries on any smooth surface  in a child under age 3 years. For children ages 3 to 5 years of  age, S-ECC is characterized by a dmfs  >1 on the smooth surface  of  the primary maxillary anterior teeth, or a dmfs  of  > 4 (age 3 years), >5 (age 4 years), and >6 (age 5 years) (American Association of  Pediatric Dentists [AAPD], 2003). 2.1.2. Prevalence The prevalence of  dental caries in the general population has declined in recent years primarily as a result of  increased exposure to fluoride,  usually from  toothpastes (van Loveren & Duggal, 2001). Determining the "true" prevalence of  ECC has been difficult because preschool children are so challenging to access (Ripa, 1988). The reported prevalence also varies depending on the criteria used to define  ECC. Because of  the relationship between socioeconomic status (SES) and ECC, prevalence varies depending on the SES of  children surveyed. ECC is "unequally" distributed in preschool children; 25% of  the children experience 80% of  the caries (NIH, 1996). Despite these challenges, a variety of  surveys suggest that about 8% of  2-year-olds and over 40% of  5-year-olds have at least one decayed or filled  tooth (Vargas, Crall, & Schneider, 1998; Ramos-Gomez, Weintraub, Gansky, Hoover, & Featherstone, 2002). The prevalence of  ECC in Canadian children varies throughout the country. Children aged 9 months to 5 years of  age in Toronto had a prevalence of  7.4% (Budowski, 1989). Preschool Inuit children in the Northwest Territories had a much higher prevalence of  65% (Albert, Cantin, Cross, & Castaldi, 1988). In B.C., Derkson & Ponti (1982) found  a prevalence of  ECC of  3.2% amongst 9 month to 6 year olds in Vancouver. Recent screenings throughout B.C. by community dental health staff  found  that ECC affected  11% of  kindergarten children surveyed with a range from  7.9% to 27.4% depending on the region (Bassett, McDonald, & Woods, 1999). Caution is suggested in comparing these figures  because of  the differing  definitions  of  ECC used by each group of  investigators mentioned above.. 2.1.3. Biological Risk Factors Dental caries is an infectious  and transmissible disease (Krausse, 1965) with a multifactorial  etiology. It requires three primary factors:  cariogenic microflora,  substrates, and susceptible tooth and host (Krausse, 1965). Substrate is fermented  by cariogenic microflora  which leads to a lowered oral pH. Depending on the tooth's susceptibility and host's antibacterial and buffering  abilities in the saliva, this decreased pH may lead to enamel demineralization (Keyes & Jordan, 1963). The three primary factors  required for dental caries to occur will now be discussed in detail. Microflora Mutans streptococci (MS) is the species of  oral bacteria primarily associated with the initiation of  the caries process. MS have unique cares-inducing properties that include the ability to adhere to tooth surfaces,  to produce copious amounts of  acids by fermentation  of dietary sugars, and to thrive in low pH environments (Sheiman, 2001). The initial timing of  MS colonization in the mouths of  infants  remains controversial. Early investigators determined that MS needs a non-shedding oral surface  to colonize. They concluded that colonization follows  the eruption of  teeth (Berkowitz, Jordan, & White, 1975). Further, a discrete window of  infectivity  ranging from  19-31 months of  age for  MS was suggested (Caufield,  Cutter, & Dasanayake, 1993). However, more recent evidence suggests that these cavity-causing bacteria can be found  in the mouths of  infants prior to tooth eruption (Wan et al., 2001; Tinanoff,  Kanellis, & Vargas, 2002; Berkowitz, 2003). Early age of  initial colonization and the presence of  high levels of  MS are considered major risk factors  for  ECC (Berkowitz, 2003). A significant  increase in MS levels often precedes the onset of  ECC and salivary levels of  the bacteria have been used to predict caries risk (Brown, Driezen, & Handler, 1976; Klock & Krasse, 1979). A strong correlation has been observed between MS species and counts between a mother and her child. The mother is the usual source of  the MS and transmits the bacteria to her child by close contact and the sharing of  food  and utensils (Tinanoff  et al., 2002; Berkowitz, 2003). The concentration of  MS in the oral microflora  of  children with ECC routinely exceeds 50% of  the cultivable plaque flora  and over 10% of  the saliva flora  (van Houte, Gibbs, & Butera, 1982). In contrast, MS forms  less than 1% of  the plaque flora  in caries-free  children (Berkowitz, 1996). Further, children with ECC have been reported to have a level of  MS in plaque that is 100 times higher than that of  their caries-free  peers (Chen, 1995). Historically, lactobacilli were considered the primary bacteria in the dental caries process. However, current knowledge links the presence of  lactobaccilli in the oral cavity to the progression, rather than initiation, of  caries. Lactobacilli are commonly found  in high levels within cavitated lesions (von Houte, 1980). High counts of  MS and lactobacilli are significant  indicators of  high caries risk. Host Saliva As the main host defense  against dental caries, saliva plays an important role in neutralizing acids produced by dental plaque and in the clearance of  foods  from  the oral cavity (McGhee & Kiyono, 1993; Seow, 1998). The contents of  saliva also provide the main immunological defense  against dental caries. Infants  develop saliva secretory immunoglobulin A antibodies (slgA) at the same time that oral bacteria colonize their mouths (Seow, 1998). slgA provides specific  immune defense  against cariogenic bacteria by interfering  with bacterial attachment to the tooth surface  (Seow, 1998). Further, inhibition of  bacteria metabolic activity by slgA may also be important (McGhee & Kiyono, 1993; Seow, 1998). However, it is difficult  to correlate slgA and caries in infants and young children because their secretory responses are likely still immature (Gahnberg, Smith, Taubman, & Ebersole, 1985; Gleeson et al., 1991). Furthermore, little clinical evidence exists indicating that slgA protects against dental caries (Michalek & Childers, 1990). The flow  rate of  saliva is also an important variable in determining its significance  as a host defense.  Flow rate influences  the rate of  oral clearance, buffering  capacity, and antimicrobial activity. Since saliva flow  rate is at its lowest during the night and/or during sleep, continuous ingestion of  sugary liquids at this time is a significant  risk factor  for  ECC (Seow, 1998). Tooth maturation or defects Enamel defects,  common in the primary dentition, occur with a prevalence ranging from  13-39% in normal full-term  infants.  In preterm or low birth-weight babies, the prevalence exceeds 62% (Tinanoff  et al., 2002). Localized enamel defects  have been attributed to local trauma and infections.  Generalized hypoplasia has been associated with hereditary conditions, birth prematurity, low birthweight, infections,  malnutrition, metabolic disorders, and chemical toxicity (Seow, 1998). Enamel maturation occurs during and following  the eruption of  the primary teeth. This is a critical period for  caries susceptibility if  the immature enamel is exposed to cariogenic microflora  and frequent  ingestion of  fermentable  carbohydrates (Seow, 1998). Structural defects  in the enamel (hypoplasia) or a change in opacity further  increase the risk of  caries in primary teeth as the irregular pits and grooves on the tooth surface  increase plaque retention. As well, clearance of  food  particles may also be delayed, thereby continuously exposing the defective  and vulnerable tooth surface  to the acidic oral environment created by the bacteria (Horowitz, 1998; Seow, 1998). Although enamel hypoplasia has been hypothesized to be a risk factor  for  ECC, the role of  subclinical enamel hypoplasia remains uncertain (Seow, 1998). Substrate Cariogenicity To allow production of  sufficient  amounts of  acid by bacteria to demineralize enamel, sugars or refined  carbohydrates must be present and utilized as substrate by cariogenic bacteria (Sheiham, 2001). Dietary sugars are simple carbohydrates that include glucose, fructose,  sucrose, and lactose (found  in milk products) (Wardlaw, 1997). Refined carbohydrates are starches processed through fine  grinding and heat treatment. They are retained on the teeth for  prolonged periods and easily broken down by oral bacteria into acids that lead to enamel demineralization. Although starchy foods  alone are less cariogenic than sucrose, those starchy foods  that also contain sucrose may be as cariogenic as sucrose alone (Rugg-Gunn, 1996). The literature on caries risk can be confusing  because some studies focus  on "sugars", while others on refined  carbohydrates. Nevertheless, both substrates are considered to be risk factors  for  ECC. MS are able to utilize sugar and fermentable  carbohydrates to produce glucan polymers that promote bacterial adherence to the tooth surface  and increase the thickness of  the plaque. However, sucrose is considered the most cariogenic sugar because oral bacteria are able to use it to produce plaque dextrans which facilitate  bacterial adherence (Mikkelsen, 1996) and replace earlier-colonizing bacteria with MS (Tanzer, 1989). Opinions differ  as to whether it is the total amount or the frequency  of  sugar that is most closely associated with caries experience. The Threshold Theory suggests a recommended "safe"  maximum for  daily sugar consumption. If  the "threshold" is exceeded, caries risk is increased (Sheiham, 1991; Eurodiet Core Report, 2001; van Loveren & Duggal, 2001). However, other researchers have demonstrated that it is the frequency  and duration of  the tooth's exposure to sugar rather than the total amount of  sugar that is related to dental caries (Bowen, Amsbaugh, Monell-Torrens, & Brunelle, 1983; van Loveren & Duggal, 2001). Frequency of  snacking between meals is a risk factor  associated with ECC (Tsubouchi, Tsubouchi, Maynard, Domoto, & Weinstein, 1995). Frequent food  consumption, especially foods  containing refined  sugars, enables continual acid production by cariogenic bacteria leading to demineralization of  the tooth. Equally important, the ongoing low pH of  the oral environment does not provide the opportunity for  enamel remineralization to occur. Over time, if  demineralization exceeds remineralization, carious lesions develop and progress to frank  decay (Tinanoff  et al., 2002). Concerns regarding inappropriate baby bottle and sippy cup use are related to the frequency  of  ingesting liquids containing simple sugars. Children with ECC are more likely to be fed  with a bottle containing fluids  other than water beyond age 1, especially during sleeptime (Tsubouchi et al., 1995). The risk of  caries also increases in children who are bottle fed  until an older age due to a longer duration of  bottle use (Leverett et al., 1993; Litt et al., 1995). However, the associations between prolonged and inappropriate bottle-feeding  practices and caries rate is not absolute as some investigators have found  little to support nighttime bottle use as a major caries risk factor  (Reisine & Douglass, 1998). Nevertheless, nighttime bottle use should be discouraged as it contributes to increased contact between substrate and bacteria (Tinanoff  & Palmer, 2003). The low pH oral environment that results from  this continuous feeding  is especially devastating to the primary teeth when the baby bottle or sippy cup is used at night and at nap-time. Saliva flow  rates are reduced at night and during sleep (Seow, 1998). Another area of  debate is the potential cariogenicity of  prolonged or nighttime breast-feeding  (Kotlow, 1977; Valaitis, Hesch, Passarelli, Sheehan, & Sinton, 2000; Tinanoff  & Palmer, 2003). Although there are some anecdotal reports that this infant  feeding  practice is associated with ECC, the contribution of  other cariogenic dietary practices cannot be dismissed. Child-rearing practices such as the use of  food  to soothe the child and unrestricted access to snacks may contribute to the caries experience of  breast- and bottle-fed  children (Johnsen, 1982; Tinanoff  & Palmer, 2003). Sweetened foods,  especially beverages, require little grinding or chewing, and therefore are popular amongst children (Falco, 2001). Fruit juices and fruit-flavored  drinks can greatly contribute to ECC due to their high sugar content and acceptance by children. They are often  continually given to children in bottles and sippy cups as snacks due to their low cost and misunderstood nutritional value (Tinanoff  et al., 2002). Increased consumption of regular soda and powdered beverages has also been reported to be associated with increased caries risk in preschool aged children (Marshall et al, 2003). The cariogenicity of  cows' milk remains controversial. Although milk sugar (lactose) has been implicated in the etiology of  ECC, it is not fermented  as completely as refined sugars. The phosphoproteins in milk inhibit enamel demineralization and antimicrobial factors  such as lactoferrin 1 interfere  with oral bacteria (Losnedahl, Wang, Aslam, Zou, & 1 Lactoferrin  deprives micro-organisms of  iron and thereby inhibits their growth or kills them altogether. Hurley, 1996). As well, a-1 casein, a milk protein, concentrates in the acquired pellicle and inhibits MS adherence to the hydroxyapatite (Reynolds & Wong, 1983). Milk's role in ECC is a concern because other food  products or sugar are sometimes combined with milk. Consequently, milk can serve as a vehicle for  cariogenic substances (Imfeld,  1983; van Loveren & Duggal, 2001; Tinanoff  et al., 2002). In summary, the simultaneous presence of  cariogenic bacteria, substrate, and a susceptible tooth and host are essential to the caries process. The acidic oral environment that results from  substrate fermentation  by the oral bacteria may lead to enamel demineralization. This process depends on host factors  such as the saliva's flow  rate, \ antibacterial and buffering  capacity, and the presence of  a susceptible tooth surface. Frequent intake of  sugars or refined  carbohydrates between meals allows the bacteria to lower the pH of  the oral environment making it favorable  to enamel demineralization. Further, retentive foods  provide a continuous source of  food  for  the bacteria and therefore are also a significant  risk factor  for  ECC. As well, continuous use of  the baby bottle or sippy cup containing fluids  other than water during the day or at bedtime may also contribute to ECC. 2.1.4. Non-Biological Risk Factors Socioeconomic Status ECC disproportionately affects  children from  low-income families  (Demers et al., 1990; Litt et al., 1995; Henry, 1997). Bottle habits, use of  preventive dental services, toothbrushing frequency  and effectiveness,  and sugar consumption are behaviors that may be influenced  by socioeconomic status and are likely to have a direct effect  on caries risk (Litt et al., 1995; Douglass, 2000). The mother or caregiver's education has also been demonstrated to be a predictor of ECC (Grindefjord,  Dahllof,  Nilsson, & Modeer, 1995; Ramos-Gomez et al., 2002). As well, in industrialized countries, caries prevalence is significantly  higher in children from cultural minorities (Grindefjord  et al., 1995). Children of  new immigrant families  in Canada are often  at risk for  ECC. Many immigrant families  experience socioeconomic challenges because the parents' education and employable skills may not be fully recognized in their new country. Language may also pose a barrier to employment and, together with poverty, will affect  the family's  access to dental care. Parenting and Family Issues A lenient parenting style has been reported to be associated with increased caries risk (Kawabata et al., 1997). A variety of  behaviors are reflective  of  a "lenient parenting style". For example, children with caries may snack more frequently,  a possible indication of caregivers' indulgence towards the children. Further, children who watch television during meals are also at greater risk for  developing dental caries possibly as a result of  prolonged acidity in the oral cavity due to the extended time spent eating (Kawabata et al., 1997). As well, this habit may indicate the presence of  other poor feeding  behaviors for  the child. This practice of  indulgence may be culturally determined (Tsubouchi et al., 1995). Further, a caregiver who is less willing to tolerate stress and upset the child increases the child's risk to ECC (Weinstein, Domoto, Wohlers, & Koday, 1992; Tsubouchi et al., 1995). Children from  single-parent families  may be at increased risk for  ECC. Families in this circumstance are also more likely to be low-income. Consequently, single-parent families may be more susceptible to stress due to reduced family  support and financial  challenges, and preventive behaviors may be forfeited  for  more immediate concerns (Litt et al., 1995; Ramos-Gomez et al., 2002). Poor oral health of  the parents is also associated with increased prevalence of  caries in their children (Henry, 1997; Mattila et al., 2000). Therefore,  risk factors  to ECC related to family  circumstances may include the family's lack of  preventive information,  barriers in accessing dental care, transmission of  high counts of  MS from  the parents to their children, or inappropriate dietary practices in the family. Preventive Dentistry homecare Opinions differ  about the caries-preventive role of  toothbrushing. Some evidence suggests a strong correlation between visible plaque on the upper anterior teeth at 19 months of  age, and caries at age 3 (Demers et al, 1990; Alaluusua & Malmivirtia, 1994; Messer, 2000). Further, there are also reports that increased frequency  and parental involvement in toothbrushing decreases the prevalence of  smooth surface  caries (Winter, Rule, Mailer, James, & Gordon, 1971; Wendt, Hallonsten, Koch, & Birkhed, 1994), while other investigators have not observed this relationship (Febres, Echeverri, & Keene, 1997). As well, caregivers of  children with caries are reported to be less aware of  the need to clean the teeth at an early age and are less likely to be able and willing to cope with an uncooperative child (Tsubouchi et al., 1995). Contrary to the notion that early initiation of  toothbrushing is important in reducing caries experience, most studies have not found  a relationship between the age at which toothbrushing begins and prevalence of  ECC (Serwint, Mungo, Negrete, Duggan, & Korsh, 1993). Although regular toothbrushing may counteract the cariogenic effects  of  a child's diet, evidence suggests that children at increased risk for  ECC due to high sugar consumption or inappropriate bottle use are also more likely to have poor oral hygiene (Paunio, Rautava, Helenius, Alanen, & Sillanpaa, 1993). Further, it is more likely the fluoride  that is available in most toothpastes rather than toothbrushing that decreases caries risk (Health Education Authority, 1996; Sutcliff,  1996). Access to Fluoride Exposure to fluoride  remains the best measure to prevent dental caries (Levy, 2003) because it reduces the dissolution of  enamel, encourages enamel remineralization, and alters dental plaque by decreasing its acid production (Sheiham, 2001). Fluoride can be delivered topically and systemically through rinses, dentrifice,  and water. Good oral hygiene and regular use of  fluoride  reduce the risk of  dental decay even with frequent  sugar consumption (van Loveren & Duggal, 2001). Although there is little evidence that toothbrushing alone reduces caries, studies have shown that toothbrushing when used with fluoridated  toothpaste does prevent decay (Health Education Authority, 1996; Sutcliff, 1996; Burt & Eklund, 1999). Increased contact with the toothpaste by extending toothbrushing time and minimizing rinsing with water following  brushing maximizes the benefits  of  fluoride  in preventing dental caries (Sjogren & Birkhed, 1993; Tinanoff  et al., 2002). Unlike rinses and dentrifice,  the delivery of  fluoride  in water is ideal as no parent or child compliance is required. Unfortunately,  the percentage of  the Canadian population that has access to fluoridated  water remains low. Continued controversy regarding dental fluorosis  and the challenges in calculating the optimal daily level of  fluoride  intake have prevented universal acceptance of  water fluoridation.  This attitude is unfortunate  because water fluoridation  remains the most equitable, effective,  and efficient  means of  delivering fluoride  to a community (Slade, Spencer, Davies, & Stewart, 1996). A study of  Medicaid-eligible children in Louisiana found  that children not residing in a community with fluoridated  water were three times more likely to receive dental treatment under GA. The cost of  their treatment was double that of  children with access to fluoridated  water (CDC, 1999). Further, water fluoridation  has reduced dental decay in primary teeth by 30 to 60% (Newbrun, 1989). Finally, at an estimated average cost of  $1 CDN per person annually, water fluoridation  is extremely cost effective  (CDC, 2001). 2.1.5. Implications for  Child Health ECC has health implications that may alter a child's quality of  life.  In addition to the pain and suffering  caused by decayed teeth, ECC may affect  a child's growth and development, speech, and self-esteem  (Davies, 1998; Weinstein, 1998). ECC is a medical problem because children with this condition have been reported to grow at a slower pace than their caries-free  peers (Acs, Shulman, Ng, & Chussid, 1999). Investigators have reported that children with ECC are in the lowest 10th percentile for  weight and are less than 80% of  ideal weight (Acs, Lodolini, Kaminsky, & Cisneros, 1992). The reduced weight and height may be the result of  decreased food  intake due to pain and infection associated with dental caries. Alternatively, both the growth lag and dental caries may be the result of  poor dietary practices (Tinanoff  & O'Sullivan, 1997). Fortunately, following dental treatment, children with ECC seem to catch-up to their caries-free  peers in weight (Acs, Shulman, Ng, Chussid, 1999). ECC may result in a premature loss of  primary teeth. This loss may lead to problems in the development of  the permanent teeth and dental arches. Without the primary teeth to preserve space and guide the permanent teeth into the arch, misalignment and malocclusion of  the permanent teeth may occur. Consequently, the permanent teeth may be vulnerable to dental problems such as caries and periodontal disease (ADSBC, 2001). The psychological impact of  ECC on a child is also an important consideration. The premature primary tooth loss or malocclusion of  the permanent teeth is aesthetically displeasing (ADSBC, 2001), and therefore  may affect  a child's self-confidence. ECC also affects  a child's quality of  life.  The chronic pain caused by ECC may affect  a child's ability to eat and sleep. Further, poor nutrition and sleeplessness may affect behavior and ability to learn. Investigators at Montreal Children's Hospital reported that prior to dental treatment under general anesthetic, 43% of  children had difficulty  eating and 35% of  children had problems sleeping. Dental treatment improved both of  these problems significantly  with 59% of  the children eating more and 84% sleeping better following treatment (Low, Tan, & Schwartz, 1999). ECC, a disease with a complex etiology, may have a profound  effect  on a child's life. The pain and infection  that may result from  dental decay have implications for  behavior and a child's ability to eat, sleep, and learn. In addition, the appearance of  the teeth and normal growth may be affected. 2.2. Dietary Iron Iron, an important trace mineral, is found  in every cell of  the body. It is essential to red blood cell function.  Iron needs to be replenished from  the diet, but is likely the most difficult  mineral to obtain in adequate amounts from  the North American diet (Davis & Stegeman, 1998). It is also difficult  to get sufficient  amounts of  iron due to its low bioavailability in most foods.  Other components of  foods  such as phytates, tannin, and calcium also negatively affect  absorption of  iron. The primary function  of  iron is the creation of  heme groups that are in hemoglobin and myoglobin (Wu et al., 2002). Hemoglobin molecules in the red blood cell transport oxygen from  the lung to the cells and take carbon dioxide away from  the cells for  excretion by the lungs. Myoglobin is the iron-containing compound found  in muscle cells that binds oxygen in muscle tissue (Wardlaw, 1997). Further, iron also plays a critical role in the myelination of  the nervous system and is involved in the enzyme pathways of  cellular metabolism (Antrim, 2004). Iron is also necessary for  immune function  and assists in the liver's role in drug detoxification  (Fairbanks, 1994). 2.2.1. Requirements (for  Children) Iron requirements for  young children vary depending on age and rate of  growth (Table 1). Full-term infants  have iron stores built-up during gestation (Williams, 2001). When supplemented by breast milk or iron-fortified  infant  formula,  these stores fulfill  an infant's iron requirements until approximately 4-6 months of  age. Although breast milk does not contain a lot of  iron (0.03-0.05 mgs/100 mis), iron from  breast milk is well absorbed (Buchanan, 1999; Antrim, 2004). Because the period between 6 and 12 months of  age is a time of  rapid development, infants  require at least 7 mg of  daily iron. Consequently, for infants  solely breastfed  at that age, iron-fortified  foods  need to be introduced into the diet to meet the increasing iron requirements and to prevent iron deficiency.  Non-breast fed infants  can meet their dietary iron requirements by consuming iron-fortified  infant  formula. From ages 1-6 years, iron requirements range from  7-8 mgs per day (The National Academy of  Sciences, 2000). Although most of  the body's iron is re-used2, replenishment with dietary iron is necessary with the increases in blood volume, muscle and their tissue growth that accompany physical growth (Saarinen, 1978) and to replace the small amounts of  iron lost during cell turnover in the gastrointestinal tract, skin, hair, and urine (Carley, 2003). When the body has surplus iron, it is stored in the liver, spleen, and bone marrow, and is called ferritin  (Wu, Lesperance, & Bernstein, 2002). 2 Iron in the body is recycled when the iron from  old blood cells are scavenged by macrophages before  the blood cells are taken out of  circulation and destroyed. The iron is then returned to the storage pool to be used again (Florida State University College of  Medicine, 2004). Table 1. Iron Requirements for  Children3 Dietary DRIsa Requirement for  Absorbed Iron (gm/d) (mg/d) Age (y) Median 97.5th percentile Ear RDA Males 1.5 0.62 1.24 3.4 6.9 2.5 0.54 1.23 2.9 6.8 3.5 0.61 1.36 3.4 7.6 4.5 0.63 1.45 3.5 7.9 5.5 0.70 1.60 3.9 8.1 Females 1.5 0.64 1.25 3.4 6.9 2.5 0.63 1.30 2.7 7.2 3.5 0.59 1.32 3.3 7.3 4.5 0.65 1.45 3.4 8.1 5.5 0.64 1.52 3.4 8.4 a from  the National Academy of  Sciences, 2000 2.2.2. Bioavailability and Absorption Iron in foods  is available in heme and non-heme forms.  The human body absorbs heme iron found  in meats better than non-heme iron found  in plant foods.  Iron's bioavailability varies from  less than 2% in certain plant foods,  to 15-20% in meats, and almost 50% in human breast milk (Saarinen, Siimes, & Dallman, 1977; Yip & Dallman, 1996; Hurrell, 1997; Zimmerman, 2001). Iron bioavailability in foods  is also influenced  by the presence of  enhancers (e.g. ascorbic acid) and inhibitors (e.g. phytate, tannin, and calcium) of  iron absorption from  the diet (Davidsson, et al., 1994; Shah, Griffin,  Carlos, Lifschitz,  & Abrams, 2003). The absorption of  iron is enhanced when fruit  juice or vitamin C is consumed with iron-containing foods  (Hurrell, 1997; Zimmerman, 2001). Evidence suggests that a 50mg supplement of  vitamin C can potentially increase the absorption of  non-heme iron by three-fold  (Hallberg & Rossander, 1984; Zimmerman, 2001). Iron from  foods  high in phytates such as spinach and lentils are poorly absorbed. The bioavailability of  iron also decreases when iron-containing foods  are consumed with coffee,  tea (tannin), or milk (Hurrell, 1997; Zimmerman, 2001). Calcium also inhibits the absorption of  iron and therefore  large amounts of  calcium (>250mg) in multimineral preparations will also affect  the bioavailability of  iron (Zimmerman, 2001; Yip & Dallman, 1996). Infants  receive their dietary iron exclusively from  breast milk or iron-fortified  infant formula  until approximately 4-6 months of  age when other foods  are introduced into their diet. Because of  their rapid physical growth and limited eating capacity, toddlers and preschoolers are susceptible to iron deficiency.  Careful  meal planning is important to ensure dietary iron requirements are met. Selecting meat, fish,  or poultry as the principal protein in a meal rather than dairy products or eggs increases the iron absorption by four-fold  (Zimmerman, 2001). In addition to including iron-rich green leafy  vegetables with meals, the choice of  beverage is also important. Accompanying meals with orange juice doubles the absorption of  iron from  the meal. Conversely, milk and iced tea will decrease the iron absorption (Hurrell, 1997). 2.2 3. Iron Deficiency Prevalence Iron deficiency  (ID), the most common nutritional deficiency  worldwide, is especially prevalent among infants  and children (Zimmerman, 2001). In the United States, iron deficiency  anemia (IDA) is estimated to affect  9% of  children age 1-2 and 3% of  children age 3-5 (Antrim, 2004). In Canada, 4-5% of  non-aboriginal3 preschoolers and 14-24% of First Nations and Inuit infants  and children experience IDA (Zlotkin, 2003; Antrim, 2004). The National Nutrition Survey conducted 25 years ago reported approximately 19% of infants  and toddlers had IDA in Canada (Canadian Task Force on the Periodic Health Examination, 1979). It appears from  recent studies that the prevalence of  iron deficiency has decreased among the general population, although the incidence among high risk populations such as the First Nations is still high (Zlotkin, 2003; Antrim, 2004). The overall prevalence of  ID amongst children under 5 years of  age in BC is unknown, because most previous studies have only focused  on the children under 2 years of  age who are at greatest risk for  ID. Considering the high prevalence of  ID amongst certain populations of preschoolers, more research focused  on this age-group of  children is needed. 3 Non-aboriginal in Canada refers  to all ethnicities with the exception of  the First Nations, Inuit, and M&is. Stages There are 3 characteristic and progressive stages of  iron deficiency.  Each stage defines iron status according to the amount of  iron in each of  three compartments: storage4, transport5, and functional 6. Iron depletion, without anemia, is often  asymptomatic and although dietary history can identify  at-risk children, confirmation  requires laboratory tests that assess blood, tissue, or bone marrow for  the iron levels in each of  these three compartments. Figure  1. Stages of development of iron-deficiency. First Stage Second Stage Iron Depletion Iron Deficient Loss of storage iron Loss of circulating iron Erythropoiesis Third Stage Iron-Deficiency Anaemia Decreased Hemoglobin production itllllll * Transport Iron 4 Total Iron Binding Capacity ^ Zinc Erythrocyte Protoporphyrin » . . k. * Hemoglobin | Mean Cell Volume ^ Mean Cell Hemoglobin 4 Zinc Erythrocyte Protoporphyrin mmm^ Adapted from "Iron Status in a Group of 9 Month Old Infants," by D. N. Lwanga, Unpublished master's thesis, p. 18, University of British Columbia, Vancouver, British Columbia, Canada. 4 Iron is stored in the bone marrow and liver and its level can be determined by measuring serum ferritin (Zimmerman, 2001). 5 Transport iron plays a critical role in the oxygen transportation and can be found  in red blood cells as hemoglobin (Zimmerman, 2001). 6 In the functional  compartment, iron is found  in myoglobin cells (stores oxygen in muscle cells that are released to provide energy during physical activity), and is also involved in energy production and enzyme function  (an essential cofactor  for  several enzyme systems) (Zimmerman, 2001). Iron depletion. Iron depletion occurs when dietary intake of  iron is inadequate for  hemoglobin synthesis and iron stores must be used. This stage is asymptomatic and iron transport and functional roles are unaffected.  Erythropoiesis is not overtly affected.  This condition escapes detection by hemoglobin or hematocrit7 screening (Carley, 2003). Iron depletion can be clinically determined through measuring serum ferritin,  a storage protein. Ferritin is a sensitive marker of  iron storage and decreases as iron stores diminish. A serum ferritin  level less than 12 |xg/L is indicative of  iron depletion. The ferritin  level, however, is increased by acute inflammation  (Lesperance, Wu, & Bernstein, 2002) and varies greatly throughout childhood (Geaghan, 1999). A low serum ferritin  of  less than 12 (o,g/L, however, is a sensitive and specific  marker of  deplete iron stores. In children where insufficient  iron stores in the bone marrow continue to diminish, iron deficiency  erythropoiesis may occur. Iron deficiency  erythropoiesis (IDE). In iron deficiency  erythropoiesis (IDE), iron stores are significantly  reduced and hemoglobin synthesis is affected  (Carley, 2003). IDE status can be determined by assessing the zinc protoporphyrin (ZPP)8 in red blood cells. A blood test with a ZPP greater than 70|xmol/mol is likely indicative of  IDE. The ZPP value is preferable  in screening for  IDE as it is not affected  by anemia related to blood loss, although this is unlikely in children in 7 Hematocritic screening measures the percentage of  whole blood that is comprised of  red blood cells. Both the number and the size of  the red blood cells are measured. 8 Protoporphyrin is a heme precursor that normally binds with iron to form  hemoglobin. In IDE, deplete iron stores result in the accumulation of  protoporphyrin. This excess proptoporphyrin combines with zinc forming ZPP. Consequently ZPP increases with inadequate iron supply (Gibson, 1990; Lwanga, 1996). Canada. However, ZPP is decreased by conditions such as lead poisoning and chronic inflammation  (Lee and Nieman, 2003), although lead poisoning is extremely rare among infants  and children in Vancouver. Other indicators of  IDE include an increase in the total iron binding capacity (TIBC) due to greater free  binding sites on the plasma iron transport protein (Gibson, 1990; Oski, 1993; Lwanga, 1996). If  left  untreated, IDE may progress to become iron deficiency  anemia. Iron deficiency  anemia (IDA). Children with iron deficiency  anemia, the most advanced stage of  iron deficiency,  have insufficient  iron stores to maintain hemoglobin production. At this stage, clinical manifestations  of  ID are likely to be observed. Indices of  IDA include a serum ferritin  level less than 12 jig/L and a blood ZPP greater than 70 jxmol/mol. There is also a decrease in the mean cell volume (MCV), a measure of  the red blood cell size (i.e. smaller cells have less hemoglobin) (Gibson, 1990). Clinically, a blood test on a child with IDA will reveal a decrease in mean cell hemoglobin (MCH), a measure of  the average weight of  hemoglobin in each red blood cell, and characteristic microcytic, microchromic ells (Antrim, 2004). Low hemoglobin (Hgb) and hematocrit values are also present in these children. Hgb levels that are more than 2 standard deviations below the normal mean for  age are observed in IDA (Wu et al., 2002). The Hgb level can be used to classify  the severity of  IDA as mild, moderate, or severe (DeMaeyer, 1989; Michaelson et al., 2000). Prolonged IDA can lead to detrimental and possibly irreversible cognitive and physical consequences for  an infant  or young child (Table 2). Further clinical signs and symptoms will be discussed in Table 2. Classification  of  Iron Deficiency  Anemia Classification Haemoglobin  level  (g/dl) Severe <7 Moderate < 10 (in children aged between 6 months and 5 years) < 9 (in infants  less than 6 months) Mild 1 0 - 1 1 Risk Factors Child's age. Young children are vulnerable to develop iron deficiency  due to 1) their high dietary needs during rapid growth, 2) their low intake of  dietary iron, and 3) their high consumption of  cows' milk and other foods  that inhibit the absorption of  iron (Michaelson et al., 2000). From ages 4 to 12 months, an infant's  blood volume doubles. However, their iron stores are often  depleted by 6 months of  age. Consequently, sufficient  intake of  dietary iron is critical during this period of  rapid growth and red blood cell synthesis (Saarinen, 1978). The small amounts of  food  young children consume and their selective food  choices may further  compromise their ability to satisfying  their high dietary iron requirements. Consequently, to maintain a healthy iron status, iron-rich foods  must be emphasized in a child's diet (Zimmerman, 2001). However, babies fed  with iron-fortified  formula throughout the first  year will enter their second year of  life  with high iron stores, and thereby masking the effect  of  their diet. Socioeconomic status. Children from  families  with lower socio-economic status are at increased risk for  iron deficiency  (Lehmann, Gray-Donald, Mongeon, & Di Tommaso, 1992). In the U.S., the NHANES I study (1968-1973) reported that IDA prevalence amongst 12 to 36 month-old children from  low-income families  was 21% compared to 7% of  children from  higher-income families  (Dallman, Yip, & Johnson, 1984). This difference  in prevalence can be reasonably attributed to differences  in feeding  practices and dietary intakes of  iron (Greene-Finestone, Feldman, & Luke, 1991). These differences  may include the amount of milk consumption as well as the intake of  iron-rich foods  such as meat, fish,  and poultry. Further, feeding  practices that affect  the choice of  beverage accompanying meals will affect  iron absorption. For children that are not receiving adequate iron through foods,  a daily intake of  a 5-10 mg iron supplement is important to ensure iron requirements are met (Zimmerman, 2001). Children of  some ethnic backgrounds may be at greater risk for  iron deficiency  as a result of  cultural differences  related to food  consumption, prolonged bottle feeding, language barriers, and socioeconomic factors  (Buchanan, 1999). Although the Canadian Task Force for  Periodic Health Examination (1994) has considered infants  of  Chinese descent to be at increased risk for  IDA, other studies have not found  IDA to be more common amongst Chinese children (Sargent, Stukel, Dalton, Freeman, & Brown, 1996; Innis, Nelson, Wadsworth, MacLaren, & Lwanga, 1997). Canadian studies have also suggested that children from  First Nations and Inuit descent are also at increased risk for IDA with a prevalence of  14% and 24% respectively (Zlotkin, 2003; Antrim, 2004). This risk may be attributed to dietary practices that include increased consumption of  beverages (especially milk or soft  drinks) and of  foods  that are poor sources of  iron. Health conditions. Although less common than dietary factors  amongst infants,  other causes of  ID include stomach conditions that greatly decrease gastric-acid secretion and reduce the body's ability to absorb iron such as prolonged achlorhydria9 (Zimmerman, 2001; Conrad, 2003). Other causes of  ID include conditions associated with gastrointestinal blood loss, such as milk protein allergy or parasitic infections  (Sullivan, 1993). Small but chronic blood loss from  the gastrointestinal tract may, over time, result in ID (Zimmerman, 2001). Early feeding  with cows' milk (before  12 months) place infants  at increased risk for  IDA due to the milk's poor bioavailability and high calcium. Infant  formula  is expensive and not always readily available in remote areas. Premature infants  are also more susceptible to iron deficiency  as they may not have an adequate gestational store of  iron at birth. Further, chronic illness reduces the body's ability to mobilize iron from  stores and consequently, the iron supply to the bone marrow for hemoglobin synthesis is also reduced. During chronic illness, food  intake is often  reduced as is the intake of  heme-containing meats. The mobility and transfer  of  iron stores is also limited by deficiencies  in vitamin A, vitamin B6, and copper (Zimmerman, 2001). 9 Achlorhydria is the abnormal deficiency  or absence of  hydrochloric acid in the gastric juices of  the stomach. Since hydrochloric acid is necessary for  protein digestion, achlorhydria may result in impaired digestion and absorption. Children with small amounts of  lead in their body may also have impaired hemoglobin synthesis that can progress to ID. Since lead and iron share the same absorption pathway and iron absorption is enhanced during ID, lead is more readily taken up by the body and can further  aggravate the anemia (Michaelson et al., 2000). However, elevated blood lead is not a problem amongst Vancouver children. Child's feeding  practices. Diets poor in iron are the most common cause of  iron deficiency  in infants  and young children (Buchanan, 1999). Breast-fed  infants  over 3-6 months of  age who are not given iron supplements or foods  with sufficient  iron are at increased risk for  ID (Innis et al., 1997). Excessive consumption of  cows' milk may also result in ID because cows' milk contains little iron, and the iron is of  low bioavailability. In addition, because it is difficult for  infants  under 12 months of  age to digest the milk protein in cows' milk, some investigators suggest that large intakes of  milk at this age can lead to a loss of  iron through gastrointestinal bleeding (Fomon, Zeigler, Nelson, & Edwards, 1981; Zimmerman, 2001). Gastrointestinal blood loss due to cows' milk feeding  doesn't seem to be a problem in children over 1 year of  age; it is recommended that infants  under 1 year of  age not be given cows' milk. Further, infants  and children consume relatively large quantities of  milk and milk products and plant-based foods  such as cereals, breads, and pastries which require little chewing. However, these non-heme foods  have low iron bioavailability compared to the heme in meat (Zimmerman, 2001). Children on vegan diets are especially susceptible to ID because most non-heme sources of  iron have low bioavailability. For these children, careful  dietary planning that includes vitamin C and iron-rich plant foods  such as whole grains, dried fruits  and nuts, and legumes are important to ensure adequate dietary iron (Wardlaw, 1997). Implications for  Child Health 'i Iron deficiency  poses a serious health concern in infants  and young children. It can lead to altered cognitive and physical development that lasts beyond the duration of  the nutrient deficit. Cognitive concerns. The growth and development of  the central nervous system (including brain growth, dendritic aborization and myelination) occurs most rapidly from  the second trimester until 18-24 months of  age (Dobbing, 1990; Williams, 2001). Inadequate iron during this critical period of  development may result in reduced essential metabolic pathways in the brain. Consequently, this reduction increases the child's risk for  impaired cognitive development (Grindulis, Scott, Belton, & Wharton, 1986; Moffatt,  Longstaffe,  Besant, & Dureski, 1994; Lozoff,  Brittenham, Wolf,  & Jimenez, 1996; Williams, 2001), poor educational performance  (Lozoff,  Jimenez, & Wolf,  1991; Hurtado, Claussen, & Scott, 1999), and lower test scores for  motor development milestones (Lozoff  et al., 1987). Evidence suggests that ID also alters a child's emotional state. Deficient  children may be more withdrawn, inattentive, and tired. These children also have decreased activity and involvement when presented with stimuli (Walter, Andraca, Chadud, & Perales, 1989; Michaelsen et al., 2000). Although the association between iron deficiency  and low developmental test scores may be due to confounding  factors  such as poor socioeconomic situation or other nutrition-related conditions, iron deficiency  likely results in the delays of mental development as described (Williams, 2001). Investigators have reported that the cognitive and physical delays associated with ID in infants  persevere despite iron therapy and the elimination of  anemia. Children with a history of  ID as infants  continue to achieve lower test scores than their peers even 10 years following  their treatment as infants  (Lozoff,  Jimenez, Hagen, Mollen, & Wolf,  2000). However, correcting the anemia in preschool children has led to marked improvements in the learning difficulties  associated with IDA. The child's age at the time of  the deficit  and the duration and degree of  the ID are critical in determining the child's risk of  permanent developmental delays (Parks & Wharton, 1989; Michaelsen et al., 2000). Physical concerns. Iron deficiency  may also hinder physical growth. This effect  on growth may be linked to changes in eating behavior due to a loss of  appetite (Levitsky & Strupp, 1995; Zimmerman, 2001; Carley, 2003), or to behavioral alterations associated with IDA (Lozoff  et al., 1998). ID may be associated with abnormal gastrointestinal (GI) function  leading to inflammation  of  the oral mucosa and conditions such as hypochlorhydria, malabsorptive syndromes, and GI bleeding (Baynes & Bothwell, 1990; Zimmerman, 2001). Further, the intestinal mucosa can become leaky and result in a loss of  iron and other nutrients (Antrim, 2004). ID may also increase the child's susceptibility to infection  because of  lowered cell-mediated immune resistance. Consequently, children with ID may be susceptible to recurrent infections  in childhood such as frequent  colds, flu,  and ear infections (Zimmerman, 2001; Dallman, 1987). Other clinical signs associated with ID include pallor or dry skin, brittle hair, and knoilonychia (poorly-formed,  upturned nails). Children with ID also exhibit a lack of  energy and tend to fatigue  easily (Zimmerman, 2001). They may also become more clingy and irritable and have decreased interactions with their immediate environment. It is also common amongst children with iron deficiency to have breath-holding spells (Antrim, 2004). It remains unclear whether some of  these problems are the cause of  or the result of  ID, but fortunately  most can be reversed with proper treatment of  the deficiency  (Williams, 2001). 2.3. Commonality between ECC and ID ECC and ID are preventable conditions common in young children. Both conditions are most prevalent in families  with socioeconomic challenges. Ethnic minorities, new immigrants, single parent families,  and families  where parents have limited education may be at particular risk. The parents of  children with ECC or ID are likely unaware of  the causes of  these conditions or may face  barriers accessing preventive resources. Moreover, poor diet and inappropriate feeding  practices are significant  contributors to both ECC and iron deficiency.  Furthermore, both children with ECC and ID tend to have similar patterns of  excessive beverage consumption (Skinner, Carruth, Bounds, & Ziegler, 2002; Levy, Warren, Bronffitt,  Hillis, & Kanellis, 2003). Large amounts of  fluids  displace the children's appetite for  iron-rich and less cariogenic foods.  Despite these possible shared risk factors, no definitive  studies have yet been done to investigate whether ECC and ID share similar dietary patterns. Establishing that there is a dietary link between the two conditions may bring increased commitment to prevention of  both conditions from  all healthcare providers who work with young children and their families.  Such an intersectoral approach to preventing both these conditions may eventually result in a decreased prevalence of  both ECC and ID in high risk children. Chapter 3 3. METHODS 3.1. Overview of  Study This two-stage, cross-sectional exploratory study targeted children between the ages of 18 months and 5 years residing in Vancouver, British Columbia. Ethics approval for  this study was received from  The University of  British Columbia's Clinical Research Ethics Board and the Children's and Women's Health Centre of  British Columbia's Research Review Committee (Appendix A). 3.1.1. Planning the Study An interdisciplinary group of  researchers and community health staff  developed and planned this study. The team included dentistry, nutrition, and speech and language professionals  from  academic, community, and research backgrounds. Numerous meetings were held to determine and refine  the objectives and design of  the study. As well, issues related to recruitment including the target population, venues for  recruitment, and incentives for  participation were discussed. The location, protocol, and implementation of the Stage 2 Dental and Nutrition Clinics were discussed and revised over several meetings. Meetings continued to be held throughout the project for  ongoing feedback  and to ensure all team members had current knowledge of  the study's progress (Appendix B). 3.1.2. Stage 1: Recruitment Between January and May 2003, children and their parents were recruited from  a variety of  community locations in Vancouver. Children participating in a public dental health program ("Smile-to-Smile Knee-to Knee") operated by dental staff  from  the North Community Health Office  of  Vancouver Coastal Health were invited to participate. As well, parents of  children from  local daycare centers and parents attending food  depots were recruited. Speech-language pathologists affiliated  with Vancouver Coastal Health assisted in the recruitment process by introducing the study to their young clients and parents. Parents of  potential subjects were approached at the community location by study investigators (ZV & AS) and were given a brief  overview of  the study. Those parents who expressed interest in participating with their children signed a consent form  (Appendix C). After  completing the consent form,  parents completed a screening questionnaire (SQ) about their child's dietary habits and food  preferences,  toothbrushing habits, and family  socio-demographics. This questionnaire concluded with an invitation for  the parent and child to participate in the second stage of  the study, the Dental and Nutrition Clinic. Interested parents provided their contact information  so an appointment could be scheduled for  the second stage of  the study. 3.1.3. Stage 2: Dental and Nutrition Clinics Parents who indicated interest in participating in the second stage of  the study were telephoned by a study investigator (AS) to set up an appointment. If  a parent agreed to participate, the parent and child were appointed to one of  four  clinics scheduled at the North Community Health Office.  Appointments were scheduled every 10 minutes from 9am to 5pm (1 lam to 7pm for  one clinic day to accommodate working parents) on four Mondays between May 5 and June 2, 2003. Upon a parent's arrival at the clinic, an overview of  clinic activities was given and parents were asked to sign a consent form  for  this stage of  the study (Appendix C). Each parent then completed a general information  sheet that included contact information  for  the child's doctor and dentist, and a brief  medical history. Parent and child were then given a "passport" of  the "stations" they needed to attend. At these stations, the child's anthropometric measurements, usual dietary intake, oral care habits, and oral health status were assessed and documented, and venous blood was taken. The four  stations were the following: 1. "Roger Ruler": Anthropometric measurements (blood pressure, height, and weight) 2. "Amazing Apple": Food frequency  questionnaire (types and amounts of  foods) 3. "Mister Molar": Oral care questionnaire and dental exam by dentist 4. "Brave Bee": Venous blood draw 3.2. Clinical Protocol 3.2.1. Questionnaires Screening Questionnaire The screening questionnaire (SQ) (Stage 1) was developed and refined  at a series of team meetings. Designed to gather information  on the family's  socio-demographics, oral care behaviors, and feeding  practices, this questionnaire was self-administered,  but clarification  was provided to the parents by study personnel when necessary. The SQ underwent focus  group testing for  validity prior to the study; time did not permit reliability testing. Spanish, Punjabi, Chinese, and Vietnamese translations were available (Appendix D). Food Frequency Questionnaire The food  frequency  questionnaire (FFQ) administered at Stage 2 was a modification  of a questionnaire previously developed10. Our modifications  ensured better recording of dietary habits of  young children and easier administration within a short length of  time. The FFQ was designed to gather data on the food  consumption patterns of  each child (Appendix E). It was administered in a 20-60 minute interview by one of  three trained nutritionists. Models of  food  were available to assist the parents in estimating the quantity of  food consumed by their child. An interpreter was present if  the parent did not understand or 10 The FFQ used in this study was previously used by the Nutrition Research Program at the BC Research Institute. speak English. The FFQ had previously undergone testing for  validity and reliability (Williams, 2001). Oral Care Questionnaire The oral care questionnaire (Stage 2) was developed by a group of  four  dental professionals  (RH, PG, TW, & AS). This self-administered  questionnaire contained 9 questions assessing the frequency  of  dental visits, bottle-use, parental attitude towards primary teeth, and current dental homecare practices (Appendix F). The questionnaire was focus  group tested for  validity. 3.2.2. Clinical Assessments Anthropometrics Height and weight were measured and recorded by a trained project staff  person on a balance beam scale. The child remained fully  clothed and removed only his/her shoes. Blood pressure was measured on the upper part of  the child's arm using an automatic blood pressure monitor with a child-size cuff  (Appendix G). Dental Examination One dentist (PG) completed dental exams on all children. This exam was conducted either in the dental chair or using the knee-to knee position (depending on the age and cooperation of  the child). A dental light, mirror, and explorer were used for  all exams. No radiographs were taken. The extent and severity of  dental decay was assessed using a modification  of  the "iceberg" model of  caries experience (Pitts, 1997). Plaque was categorized as "light" or "heavy" according to the amount present on teeth surfaces  51 buccal, 54 buccal, and 84 lingual (Appendix H). Blood Work Assessments After  all the questionnaires and the dental exam were completed, venous blood was taken from  the children by a phlebotomist. All vials used in gathering the blood work were pre-labeled with the child's pre-assigned subject code. Blood analysis occurred later that same day at the Children's & Women's Health Centre of  British Columbia. 3.2.3. Data Analysis All subjects were assigned a subject identification  number. The questionnaire and clinical data for  all the children was entered on a Microsoft  Excel spreadsheet. Frequency tables were generated and some variables (e.g. children's age) were plotted to assess their distribution. Some categories were collapsed when appropriate (e.g. the three categories for family  income of  <$20,000, $20,000-$50,000, and >$50,000 were collapsed into <$20,000 and >$20,000). The Statistical Package for  the Social Sciences (SPSS) was used for bivariate analysis using Chi-squares and Fisher's Exact Tests for  categorical data, and one-way ANOVA and t-tests for  continuous data. Backward logistic regression models were then created to explore significant  predictors of  caries severity for  all children. Statistical significance  was established at p=0.05. Measurements of  the height- and weight-for-age,  as well as the weight-for-stature  were compared to the Centre for  Disease Control and Prevention (CDC) Growth Charts (CDC, 2000) to determine whether the children were "low", "normal" or "high" when compared to the 75th percentile for  age and gender. The data from  the FFQ was entered into the Elizabeth Stuart Hands and Associates (ESHA) Food Processor Program and data relevant to the study were further  analyzed. This included data on total calories, sugar and fluid  consumption. The grams of  sugar intake provided by the ESHA Program's analysis of  dietary intake for  each child were converted to calories by multiplying the value by 4. Proportions of  sugar consumption to calories were then calculated by dividing the total sugar in calories by total calories consumed by the child. The blood was analyzed for  essential and toxic trace elements and serum ferritin;  In addition, a complete blood count was done. The children were categorized as "normal" (serum ferritin  >12|j.g/L) plus hemoglobin >1 lOg/L, "iron deplete (ID)" (serum ferritin <12fig/L)  plus hemoglobin >1 lOg/L, "iron deficient  erythropoiesis (IDE)" (iron deplete and ZPP >70|j.mol/mol), and "iron deficient  anemic (IDA)" (iron deficient  erythropoiesis and Hgb <1 lOg/L) according their blood work results. Analysis included collapsing the categories and evaluating the children according to "normal" and "deficient"  (iron deplete, IDE, and IDA) iron levels. Parents of  children who were iron deficient  were notified  of their child's iron status through a letter and urged to contact the child's physician. Results of  the blood work were also mailed to the child's physician. The data from  the dental questionnaire was analyzed as previously described. Each child's total number of  decayed, missing (due to decay), and filled  tooth surfaces,  "dmfs", was calculated. A child's dental health status was assessed by their dmfs  and plaque scores. Initial analysis included all 99 children from  Stage 2. However, in recognition that older children were more likely to have caries and younger children were more likely to be iron deficient,  further  analysis of  the variables was done with the sample divided into "under 36 months" and "over 36 months". This division reflected  the bimodal age distribution of  the children in the study. For the children under 36 months, caries status was represented by dmfs>0  (presence of  decay) or dmfs=0  (absence of  decay). For children over 36 months, caries status was analyzed according to the absence or presence of  caries, as well as severity of  caries. Chapter 4 4. RESULTS One hundred and ninety-one children were recruited for  Stage 1. Ninety-nine of  their parents consented to participate in Stage 2 of  the study. Only the information  gathered from the 99 "Stage 2" children was analyzed. In all cases where raw numbers and percents are presented, the percent is represented in the tables as "valid percents."11 Those few  children with missing data are not listed in the tables. Data on an extensive number of  variables were collected for  each child in the study. However, only results relevant to the objectives of  this study will be presented and analyzed. 4.1. Stage 1 Data: Screening Questionnaire (SQ) Data from  the Stage 1, Screening Questionnaire (SQ), will be presented first. 4.1.1. Demographics Demographic information  was collected in the SQ, and is presented in Table 3 for  the 99 children who returned for  Stage 2. The distribution of  the children's ages, represented by Figure 2, shows that age generally followed  a bimodal distribution. That is, the children "clustered" in two age groups: one group of  children from  18 to 36 months of  age and the remainder from  36 to 71 months. 11 "Valid percents" is a calculation based only on data with a subject response and therefore  considered "valid". Data that do not have a response are not included in the analysis. Table 3. Demographics of  Study Sample Age (months) Range 20-71 Mean (SD) 43.4 + 14.7 N  Valid  % < 36 months 35 35.4 > 36 months 64 64.6 Gender Male 62 62.6 Female 37 37.4 Ethnicity Caucasian 22 23.9 Oriental 30 32.6 Multi-ethnic/Other 40 43.5 Post-secondary education Mother Yes No Father Yes No 63 31 51 29 67.0 33.0 63.8 36.3 Total family  income < $20,000 47 > $20,000 46 50.5 49.5 From the Screening Questionnaire Figure  2. Age distribution. 18 16 14 1 2 1 10 8 6 4 2 0 20 25 30 35 40 45 44 50 55 Age 60 65 70 4.1.2. Eating Patterns Data associated with the children's eating patterns are presented in Table 4. Eating patterns include variables such as meat, fish,  and poultry consumption, and number of times a child eats something each day. Most parents (62.0%; n=59) reported that they had concerns about their child's eating. The most frequent  concerns were that the child was a "picky eater" (17.8%; n=33) and "won't try new foods"  (14.6%; n=27). According to the SQ, the children consumed an average of  3.1+1.3 cups of  milk daily, with 65.0% (n=61) of  children drinking 3 or more cups daily. The average daily consumption for  juice was slightly less at 2.8+1.4 cups with 46.5% (n=47) drinking 3 or more cups daily. Overall, all 94 children who answered the SQ consumed 3 or more cups of  fluid  (other than water) daily. Table 4. Eating Patterns from  Screening Questionnaire .12 Food security Not a concern Concern n 54 44 Valid % 54.5 44.4 Concerned about child's eating No 36 Yes 59 37.9 62.1 Meat, fish,  poultry consumption (per week) < 5 times 46 49.5 > 5 times 47 50.5 Number of  times child eats something (per day) Mean (SD) 4.9 ±1.6 <5 61 65.6 >5 32 34.4 4.2. Stage 2 Data: Dental and Nutrition Clinics 4.2.1. Anthropometrics Measurements of  the children's height and weight were used to calculate their weight-for-age,  height-for-age,  and weight-for-stature.  The z-score for  the children's weight-for-age, height-for-age,  and weight-for-stature  were compared to the Centre for  Disease Control and Prevention (CDC) Growth Charts (CDC, 2000) to determine whether the children were "low", "normal" or "high" when compared to the 75 th percentile of  their peers of  similar age or stature (Table 5). Most of  the children were normal (mean=42.7%, 1 2 "Food security" refers  to the parents' report that financial  issues affected  the quality or variety of  foods  the family  eats. n=39) or high (mean=38.2%, n=35) when compared to the 75th percentile of  children of their same age and stature for  gender. Only 19.1% (n=17) of  the children scored low compared to their peers. Table 5: Anthropometric Measurements of  Study Population (75th Percentile of  z-scores) n Valid % Weight-for-Age Low 18 19.6 Normal 34 37.0 High 40 43.5 Height-for-Age Low 18 19.8 Normal 43 47.3 High 30 33.0 Weight-for-Stature Low 16 18.0 Normal 39 43.8 High 34 38.2 *based on CDC Growth Charts: United States (2000) 4.2.2. Eating Patterns from  Food Frequency Questionnaire The FFQ provided extremely detailed information  on the types and amounts of  foods consumed by each child. For purposes of  this project, analysis of  the FFQ was limited to daily sugar consumption and types and amounts of  beverages consumed on a daily basis (Table 6 and 7). Table 6. Sugar Consumption of  Study Sample (Daily) from  FFQ All Children Calories (kcal) Range 1085.2-4856.9 Mean (SD) 2221.9 ±733.9 Sugar (g) Range 48.5 -371.8 Mean (SD) 149.5 ±63.0 % of  calories as sugar8 Range 13.0-44.0 Mean (SD) 27.0 ± 6.0 a Includes all dietary sugars (sucrose, glucose, fructose,  and lactose) and calculated by the following  formula: Sugar (g) x 4 x 100 Total Calories (kcal) In addition, beverage consumption as reported in the FFQ was analyzed (Table 7). In all, 63.6% of  children (n=63) consumed 3 or more cups of  fluid  daily according to the FFQ. Table 7: Beverage Consumption Reporting on the SQ and FFQ SQ FFQ n = 94 n = 99 Milk 3.1 ± 1.3 2.4 ± 1.7 Juice 2.8 ±1.4 1.5 ±1.4 Total 6.0 ±1.9 4.1 ±2.5 * Mean ± SD (cups per day) The patterns of  beverage consumption were also examined. Baby bottle and sippy cup use13 for  fluids  other than water was frequent  or had been a frequent  habit among the children with 59.1% (n=54) describing a history of  often  carrying a bottle throughout the day, and 40.9% (n=38) a history of  napping or sleeping with a bottle. 4.2.3. Dental Health Data on dental health behaviors is presented in Table 8. o Table 8. Dental Data from  the Oral Health Questionnaire Baby teeth are important Yes No or Not Sure Dental visits Parent's At least once every 2 years Once every 3 yrs /When something hurts/Never Child's At least once a year When something hurts/Not yet Daily toothbrushing By parent Yes No By child Yes No Use of  fluoride  toothpaste Yes No Child's teeth clean after  brushing Yes No 13 Parents were asked to report on their child's current or historical use of  the baby bottle and/or sippy cup in the questionnaire. n Valid % 83 91.2 8 8.8 47 50.5 46 49.5 51 54.8 42 45.2 61 66.3 31 33.7 73 77.7 21 22.3 68 73.9 24 26.1 37 39.8 56 60.2 4.2.4. Caries Status Results of  dental exams revealed that, as expected, caries status did not follow  a normal distribution. About 1/3 (n=35) or 35.4% of  children were caries-free  (dmfs=0).  Another 1/3 (n=32) or 32.3% had a moderate caries score, (dmfs>0  and <5). A further  1/3 (n=32) or 32.3% had high caries or dmfs>5  (Table 9). For the first  stage of  the analysis, caries-free and moderate caries children (dmfs<5)  were combined into a "low caries" group (n=67; 67.7%), and the remaining 32 children with dmfs>5  were designated a "high caries group." Chi-square or Fisher's Exact Tests were used to compare the low caries to the high caries children for  a variety of  variables. Children with high caries were significantly  more likely to be older, i.e. over 36 months of  age (Table 9). Because so few  children under 36 months of  age had severe caries (dmfs>5),  children were also grouped according to "presence" (dmfs>0)  or "absence" (dmfs=0)  of  caries to allow further  analysis of  caries status for  the younger age group (Table 8). Children with dmfs>0  were called "dmfs+"  and those with dmfs=0  were "dmfs-".  Dental plaque was also measured as either light or heavy14; 75% of  the children had heavy plaque deposits. Because of  the lack of  variation in the assessments of  plaque, these results were not analyzed further. 1 4 The definition  of  light or heavy plaque was at the discretion of  the dentist (PG) who did the dental exam on all the children. Table 9. Caries Status of  Study Sample from  the Dental Examination8 All Children Under 36 Over 36 months (n=96) months (n=34) (n=62) dmfs  (Range) 0 - 4 5 0 - 3 7 0 - 4 5 Mean (SD) 7.2 (11.3) 2.1 (6.4) 10.0 (12.4) Valid Valid Valid Severity of  caries n % n % n % Low (dmfs  < 5) 65 67.7 32 94.1 33 53.2 High (dmfs  > 5) 31 32.3 2 5.9 29 46.8 Valid Valid Valid Presence of  caries n % n % n % dmfs  - 34 35.4 21 61.8 13 21.0 dmfs  + 62 64.6 13 38.2 49 79.0 a Of  the 99 children that participated in Stage 2 of  the study, dental exams were completed on 96 of  the children. 4.3. Explanatory Variables and Caries Status The questionnaires and clinical evaluations provided detailed information  on the dietary habits, oral care, and dental status of  the children in the study. However, only data of interest to the goals of  this study was further  analyzed. 4.3.1. All children As previously described, distribution of  caries did not follow  a normal distribution. Therefore  non-parametric analyses by Chi-square tests or, when fewer  than 5 subjects in a category, Fisher's Exact Tests were done. The relationship between caries status (high or low) and the demographic, dietary, and dental health variables was explored (Table 10). However, because few  variables demonstrated a significant  relationship, only selected variables that were significant  or approached significance  are listed in the tables. Table 10. Selected Variables and Caries Status for  All Children (n=96)a Caries status dmfs<5  dmfs>5  p-value (n=65) (n=31) Demographic variables Child's age (months) Mean (SD) 38.5 (14.7) 54.4(10.2) <0.001b Gender Male 37 (56.9%) 24 (77.4%) 0.009 Female 28 (43.1%) 7(22.6%) Family income <$20,000 28 (45.2%) 18(64.3%) 0.05 >$20,000 34(54.8%) 10(35.7%) Food security Concern 25 (39.1%) 18(60.0%) 0.03 Not a concern 39 (60.9%) 12 (40.0%) Dental Daily toothbrushing by parent Yes 44(72.1%) 15(51.7%) 0.06 No 17(27.9%) 14(48.3%) Child's dental visits At least once a year 27(43.5%) 23 (76.7%) 0.003 When something hurts/not yet 35 (56.5%) 7 (23.3%) a Of  the 99 children that participated in Stage 2 of  the study, dental exams were only completed on 96 of  the children. b P-value determined by t-test (all other p-values determined by chi-square or Fisher's Test). Significant  relationships were observed between caries status and age and gender. Children with high caries were older (mean age=54.4 months; p=<0.001). As well, girls were significantly  less likely to have high caries compared to boys (p=0.009). Further, a significant  relationship was observed between family  income and caries status, p=0.05. Of those 28 children with "high caries", 64.3% (n=18) were from  a family  with an annual income less than $20,000. Only n=10 (35.7%) of  the high caries children were from families  whose annual income was $20,000 or more. Parents who reported the quality or variety of  foods  served at home was affected  by finances  (i.e. "food  security") were significantly  more likely to have children with "high caries" compared to children of parents who did not have these concerns about food  (p=0.03). A significantly  greater percent of  children with high caries (76.7%; n=23/30; p=0.003) were likely to have visited the dentist at least once a year than those with low caries (43.5%; n=27/62). Backward stepwise logistic regression was done to analyze the effect  of  a number of variables on the outcome variable, caries severity, while controlling for  other potential covariates. Preliminary models included demographic, anthropometric, dietary, bloodwork, and dental health variables. Only two variables, age and food  security remained in the final model (Table 11). Table 11. Logistic Regression of  Select Variables of  Significance B S.E. Wald df Sig. Exp (B) Age 0.099 0.026 14.268 1 0.000 1.104 Food security 1.861 0.660 7.945 1 0.005 6.432 Dental IQa 0.373 0.202 3.425 1 0.064 1.452 Constant -7.806 1.712 20.797 1 0.000 0.000 a Dental 1Q includes the following  variables: parent's and child's dental visits, use of  fluoride supplements or toothpaste, if  the child's teeth are clean following  brushing, and whether the child sleeps with or carries a bottle or sippy cup. Given that caries and age were significantly  associated, caries status was further analyzed with children divided into younger (under 36 months) and older (over 36 months) children. 4.3.2. Children Under 36 Months Analysis of  caries status in children under 36 months was undertaken with presence (dmfs+)  or absence (dmfs-)  of  caries as the caries outcome variable. Because only 2 children under 36 months had high caries, severity of  caries was not an appropriate outcome variable for  this age group. None of  the variables related to severity of  caries for the entire group of  children were related to presence of  caries in children under 36 months. However, another dietary variable, the daily percentage of  calories contributed by sugar was significantly  related to presence of  caries in these young children (p=0.003; Table 12). Caries-free  children were less likely than caries-positive children to have more than 30% of daily calories from  sugar. Table 12. Sugar Consumption for  All Children Under 36 Months (n=34) Caries Status p-valuea Odds 95% CI ratio % of  Calories as Sugar dmfs-  dmfs+ < 30% 17 5 0.03 1.0 1.1-45.4 > 30% 4 8 6.8 Total 21 13 P-value determined by Fisher's Exact Test 4.3.3. Children Over 36 Months Caries status for  children over 36 months (n=62) was analyzed using both caries outcome variables: presence or absence of  caries and severity of  caries. Fisher's Exact Tests and odds ratios15 were calculated to allow further  related analysis of  predictive variables for  caries (Table 13). 1 5 Odds ratio is a statistical comparison of  whether the probability of  an event is the same for  two groups. An odds ratio of  1 can be interpreted as an equal probability of  an event occurring for  both groups while an odds ratio greater than 1 implies that the event is more likely to occur in that group. An odds ratio of  less than 1 implies the event is less likely to occur in that group. Table 13. Select Variables of  Caries for  Children Over 36 Months (n=62) dmfs  + dmfs  - p-value4 Odds ratio 95% CI dmfs  < 5 dmfs  > 5 p-value* Odds ratio 95% CI Income <$20,000 30 3 0.01 5.6 1.1 -30 .9 15 18 0.15 0.4 0.1-1.3 >$20,000 16 9 . 1 17 8 1 Food Security Yes 26 4 0.08 2.7 0 . 8 - 9.2 12 18 0:06 3.2 1.1-8.9 No 22 9 1 21 10 1 Daily milk (cups/day)c <3 32 12 0.05 1 1.0-40.7 27 17 0.08 1 1.0-9.8 >3 17 1 6.4 6 12 3.2 Total fluids  (cups/day)c <3 14 6 0.09 1 0 . 6 - 12.8 13 7 0.2 1 0.8-7.3 >3 32 5 . 2.7 16 21 2.4 Sugar Consumption^ <50% 7 5 0.05 1 1.0-14.2 6 4 tvtf 1 0.3-6.8 >50% 42 ; 8 3.8 27 25 1.4 *P-value determined by Fisher's exact test. k P-value determined by Chi-square test. c Values for  daily milk and total fluid  consumption from  food  frequency  questionnaire. 4 Includes all dietary sugars (glucose, sucrose, and lactose) and calculated by the following  formula:  Sugar from  all fluids  and sugary snacks (g) x 100 Total sugar (g) Annual family  income was related to caries-free  status. Children from  families  who reported a total household income of  less than $20,000 were more likely to have caries (p=0.01). Severity of  caries and income were not significantly  related (p=0.15). The association between families  that reported no concerns about food  security and low caries also approached significance  (p=0.06). While family  income was the only significant  demographic variable, dietary variables of significance  included daily milk and sugar consumption. Total milk consumption according to the FFQ was also associated with caries. Children who drank less than 3 cups of  milk daily were more likely to be caries-free  (37.5%; n=12) compared to children who consumed more than 3 cups of  milk (5.9%; n=l) (p=0.05). Sugar consumption was associated with caries experience for  children over 36 months. Children with diets that had sugar constituting 50% or more of  their daily calories were more likely to have caries (p=0.05). Increased intake of  milk and consumption of  beverages and snacks containing a high percentage of  sugar were associated with caries in the older children in the study (Table 13). 4.4. Iron Store Status For iron stores, 75.0% (n=72) of  children had normal stores and 25.0% (n=24) of children were iron deficient.  Among the children with iron deficiency,  58.3% (n=14) were iron deplete, 25.0% (n=6) had iron deficiency  erythropoiesis (IDE), and 17% (n=4) had iron deficiency  anemia (IDA) (Figure 3). Children under 36 months had a significantly higher prevalence of  iron deficiency  compared to children over 36 months (p<0.05) (Table 14). Figure  3. Prevalence of iron deficiency stages In study sample Iron Deplete Iron Deficiency Bythropoiesis Iron Deficiency Anemia Q All Children (n=24j • Under 36 Months (n=13) o Over 36 Months tn=11) p = 0.05 X 2 = 4.91 Table 14. Iron Store Status of  Study Sample from  Blood Analysis All Under Over Children Valid 36 months Valid 36 months Valid n % n % n % p-value Chi-square Normal 72 75 21 61.8 51 82.3 0.05 4.91 Deficient 24 25 13 38.2 11 17.7 4.5. Explanatory Variables for  ID The initial analysis explored all the children in the study by iron store status (normal versus iron deficient).  Because children less than 36 months were more likely to be ID (p=0.05) than older children, younger and older children were then analyzed independently. 4.5.1. All Children This analysis included all 99 children in Stage 2 of  the study and compared children with normal iron stores (n=72) to those with iron deficiency  (n=24). Children's dental visits was significantly  related to iron status (p=0.01). Children with ID are less likely to visit the dentist at least once per year. Iron status was not significantly  related to any socioeconomic or anthropometric variables, although gender approached significance,  p=0.06 (Table 15). ID appeared to be more common in girls. Because no variables appeared to be significantly related to ID other than dental visits, odds ratios were not calculated. More complex multivariate analysis, e.g. logistic regression, was not done. Those explanatory variables that demonstrated an association with caries status for  all children did not show such an association with iron status. ( Table 15. Select Variables of  Iron Status for  All Children (n=99) Iron Status Normal Deficient  p-valuea  n=72 n=24 Demographic variables Child's gender Male 49 (68.1%) 12 (50.0%) 0.06 Female 23 (31.9%) 12 (50.0%) Family income <$20,000 35 (52.2%) 12 (52.2%) 0.09 >$20,000 32 (47.8%) 11 (47.8%) Food security b Concern 32 (44.4%) 12 (52.2%) 0.2 Not a concern 40 (55.5%) 11 (47.8%) Dental Child's dental visits At least lx/year 42 (61.8%) 7(31.8%) 0.01 When something hurts/not yet 26 (38.2%) 15(68.2%) a P-value determined by Chi-square or Fisher's Test. b The number of  children included in each variable may not total 99 due to non-responses. Although Chi-square analysis failed  to show any relationship between cups of  milk per day and iron status, a one-way ANOVA demonstrated significant  differences  in milk consumption between children at increasing stages of  iron depletion (Table 16). As children's iron status worsened, milk consumption significantly  increased. This trend was also observed with total fluid  consumption, but was not statistically significant.  However, given this relationship was observed with milk consumption reported in the SQ, no further post-hoc analysis was done. This finding  was not replicated when the FFQ beverage consumption was analyzed. Table 16. Iron Stores & Milk and Total Fluid Intake # Milk [cups/day] (SD) Total Fluid [cups/dayl (SD) Normal 71 2.9(1.4) Deplete 14 3.0(1.4) Deficient  6 4.0(1.1) Anemic 3 4.7(1.5) 5.7 (2.3) 5.9(1.8) 6.5(1.6) 7.3(1.5) F-Stat=2.7, p=0.05 F-Stat=0.9, p=0.5 a Values for  daily milk and total fluid  consumption from  the screening questionnaire. 4.5.2. Children Under 36 Months No statistically significant  relationships were found  between iron status and any of  the demographic, anthropometric, and socioeconomic variables that were analyzed in children under 36 months of  age. However, total daily milk consumption from  the SQ was related to iron store status for  children under 36 months (p=0.03; Table 16 and 17). Iron deficient children were more likely to consume 3 or more cups of  milk per day. Table 17. Daily Milk Consumption and Iron Status for  Children Under 36 Months (n=34) Iron Status p-value Odds ratio 95% CI Milk (cups)/day Deficient Normal 3> 8? "3 .5 s a a O) S u <3 > 3 2 11 11 10 0.03a 1 6.1 0.9-51.7 U 8 1/3 3 o> Total 13 21 u « e .b <3 6 13 0.3b 1 0.5-7.5 g « 2 1 to •o « O 3 o o< to > 3 Total 7 13 8 21 1.9 a P-value determined by Fisher's Exact Test b P-value determined by Chi-square Test Again, this result was not confirmed  when the FFQ data were analyzed in the same manner. 4.5.3. Children Over 36 Months None of  the anthropometric, socioeconomic, or dietary variables that we analyzed appeared to be associated with iron status in the older children. Chapter 5 5. DISCUSSION 5.1. Limitations of  the Study Prior to discussing the findings  of  this cross-sectional, exploratory study some limitations related to study design and implementation of  the study will be reviewed: • Sampling method and recruitment strategy • Age range of  participants • Social desirability bias • Screening questionnaire • Food frequency  questionnaire 5.1.1. Sampling Method and Recruitment Strategy If  the goal of  the study was to determine the prevalence of  disease in the general population, a random sample of  Vancouver children would have been recruited. However, given that the goal of  the research was to explore a possible relationship between early childhood caries and iron deficiency  by investigating common dietary patterns, and that both of  these conditions are prevalent in low-income and ethnic minority children, our recruitment targeted sites frequented  by low-income families  (Dallman et al., 1984; Demers et al., 1990; Gary-Donald, Di-Tommaso, & Leamann, 1990; Litt et al., 1995; Henry, 1997). Therefore  our sample was non-random and purposive. The sample also consisted of volunteer parents (selection bias). However, this deliberate recruitment strategy limited our ability to generalize the study's results to the entire population of  Vancouver children. As well, the 99 children and their parents who agreed to participate in the second stage of  the study may not reflect  the general population (participation bias). Of  the 191 parents who were approached and agreed to participate in the first  stage of  the study, only one-half  continued to the second stage. More parents might have participated in a one-stage design. However, it was not reasonable to implement all the questionnaires and clinical assessments at the recruitment locations (i.e. food  depots, daycares). Parents who took the time to participate may have been more motivated and aware of  child health concerns. Further, the sample of  99 subjects who ranged from  early childhood to kindergarten age proved to be too small to draw conclusions about two conditions that affect  different  ends of  the preschool age spectrum. A more limited age range of  children, e.g. 3 years and under would have better fulfilled  the goals of  our study. 5.1.2. Age Range of  Participants The extensive age range of  the participants in the study was a limitation. The range from 18 to 71 months of  age represents a lengthy period of  growth and development. Because of this time of  rapid change, dietary intake and practices likely differed  greatly between the younger and older children in the study. The Canadian Food Guide recommends that, although preschoolers (ages 2-5) require similar variety of  foods,  the amounts consumed depend on age, body size, activity level, growth rate, and appetite. Further, the younger children were at greater risk of  iron deficiency  while the risk of  caries was greater in the older children. This variation in risk and the broad age range made it challenging to study the common risk factors  of  these two conditions. 5.1.3. Social Desirability Bias Questionnaires that require retrospective reflection  are vulnerable to recall bias. Consequently, it was difficult  to be sure of  the accuracy of  the parents' responses to all of our questionnaires. For example, responses to the oral homecare questionnaire suggested a "high dental IQ", i.e. that parents knew expected answers. Parents may have provided "expected" answers which may not necessarily have been accurate reflections  of  their homecare practices. Parents gave responses that they knew were desirable, but not necessarily what they did. As well, the nature of  some of  the questions made the questionnaires susceptible to "socially desirable" responses. The interview format  of  the FFQ may also have been prone to this social desirability bias because the presence of  the nutritionists who administered the questions may have affected  the parents' response. Parents wanted to give the "right" answer. Although the screening questionnaire was translated into multiple languages, attaining informed  consent, and completing the food  frequency  and homecare questionnaires were challenging when the parents had a limited understanding of  English. Moreover, it was difficult  to assess whether any biases were introduced with "on-the-spot" verbal translation of  the questionnaires 5.1.4. Screening Questionnaire The screening questionnaire (SQ) was mainly a tool to recruit subjects and generate i interest in the project, rather than a reliable instrument for  gathering data. The SQ was tested in focus  groups for  validity, but its reliability was not established. Although results from  the SQ demonstrated some significant  relationships (e.g. iron deficiency  and cups of milk), lack of  reliability testing and concerns about the environment where the SQ was completed probably resulted in some measurement error. However, the demographic data collected was probably reasonably correct. 5.1.5. Food Frequency Questionnaire In contrast, the FFQ had been used in previous research and shown to be able to rank infants  in relation to sources of  dietary, iron intake and status (Williams, 2001). The FFQ provided information  on the types, amounts, and frequency  of  food  consumed over a one day, one week, or two week period. Although collaborative studies have many benefits,  the type of  dietary data needed for  our study of  dental health did not suit the objectives of  other study investigators. Because of  this, daily frequency  of  intake was not entered. A more specific  record outlining the daily frequency  of  eating and time of  consumption during the day such as obtained by a 24 hour food  recall, or a prospective food  record would have been more useful  to us. For children with ECC, the frequency  that bacteria are in contact with cariogenic substrates, the way cariogenic foods  are consumed, and the retentiveness of foods  are more significant  than total quantity of  food  consumed over an extended period of time (Serwint et al, 1993). The FFQ assessed children's food  consumption patterns as recalled by their parents. Unfortunately,  this method of  collecting dietary data tends to overestimate the food consumption (Hankins et al., 1970). As well, it was uncertain whether the dietary data recorded reflected  the type and quantity of  food  served by the parents or the actual food consumed by the child. It was anticipated that parents would "over-report" in the FFQ, however beverage consumption was lower than what was reported on the SQ. Perhaps milk in a bottle was not seen by parents as necessary information  to include in the FFQ. Again, this finding  likely reflects  the dubious accuracy of  the SQ. Parents' report on beverage consumption in the SQ did not correspond to their responses in the FFQ completed at a later date. It is difficult  to determine whether this discrepancy was due to environmental influences  during the completion of  the screening questionnaire (i.e. food  depots, daycares), recall biases, the FFQ's tendency to overestimate food consumption, or bias because the FFQ was implemented by an interview. Further, children participating in the study were undergoing rapid growth and the types and quantities of food  they consume are continually changing. Consequently, the differences  in consumption patterns between the two instruments may also be attributed to the weeks that lapsed between the completion of  the screening and food  frequency  questionnaires. In the interview, there may have been some confusion  amongst parents about which category in the FFQ corresponded to the juice that their children consumed. Further, in entering the dietary data, fruit  juice was assumed to be "100% natural and unsweetened." Since nearly half  of  the families  reported that they had "food  security" concerns, it is likely that many of  these families  opted to purchase less expensive juices that are sweetened which would directly affect  the children's total sugar consumption. Thus, sugar consumption may be under-reported in the FFQ. 5.2. Characteristics of  the Study Sample Some findings  of  interest about the children and families  in our study warrant further discussion. About twice as many boys as girls participated in the project (Table 3). This difference  was not intentional and the explanation for  this difference  is unknown. Over 75% of  the children were from  ethnic minorities16 and over 50% of  the families  had an annual income of  less than $20,000 (Table 3). According to Statistics Canada's after-tax low income cut-off  (LICO) for  a family  of  three in 2000 is $23,415. Compared to Statistic Canada's 2001 Census which reported that 20.8% of  families  in Vancouver live below the LICO, the fact  that more than half  of  the families  in the study were below the LICO was troubling, but not unexpected. The disproportionate number of  ethnic minority and low-income families  that participated in this study was related to the recruitment locations targeted by the study investigators. Programs in Vancouver that assist low-income families were recruitment sites for  the study (i.e. food  depots, dental health programs implemented by public health professionals). Although household income and parent's education are usually correlated (Petersen, 1992; Verrips et al., 1992; Khan & Cleaton-Jones, 1998), such a relationship was not observed in the families  participating in this study. Many of  the parents in our study were immigrants whose post-secondary education may not be recognized in Canada which 1 6 According to Statistics Canada (2001), 37% of  the Vancouver population is visible minorities. Visible minorities are defined  by the Employment  Equity Act as "persons, other than Aboriginal peoples, who are non-Caucasian in race or non-white in colour." would affect  their employment in well-paying jobs. It is troubling that so many well-educated parents are unable to earn an income above the poverty line. All children were weighed and measured. Although half  of  the children in the study were living in households with financial  challenges and most parents (62.1%) were concerned about their child's eating, the majority of  the children (80.9%) were considered normal or above average for  their weight- or height-for  age and weight-for-stature compared to the 75th percentile for  children of  their same age and gender. Only 19.1% rather than the expected 25% of  children were below normal for  their age and gender. When considering the large daily caloric intake of  the children, it is very likely that they are consuming more calories, but not necessarily more nutritious foods.  According to the CDC growth charts, children on average weigh more than they did in 1977, although their height remains the same (US Department of  Health and Human Services, 2000). This increase in weight may have implications for  the increase in childhood obesity (US Department of Health and Human Services, 2000). The screening questionnaire (SQ) gathered information  on eating patterns. Meat, fish, and poultry (MFP) consumption was investigated because of  the study's focus  on iron store status. Infants  of  nine months of  age who consume less MFP are more susceptible to iron deficiency  (Innis et al, 1997). Parents were also asked about the number of  times their child eats or drinks per day to assess the frequency  of  daily food  consumption. Other investigators have found  an increased caries risk in children that snack frequently (Tsubouchi et al, 1995). Most children ate an average of  five  times per day, which is equivalent to the recommended three meals and two snacks of  the Canadian Food Guide (2004) (Table 5). The reports of  the number of  times the children ate daily is likely an underestimation as parents were often  unsure what and how often  the children ate when they had another caregiver (i.e. spouse, relative, and daycare or preschool staff).  Previous investigators have also suggested snacking reports to be inconsistent between the children and their parents (Elkman, 1990). Further, this frequency  of  eating was surprisingly low when considering the high daily average calories for  children in this study as reported in / the FFQ (mean = 2222 kcal) (Table 6). The food  frequency  questionnaire provided extensive information  on the children's caloric intake and nutrient consumption. The mean caloric intake (2222 kcal) of  the children in the study was much higher than the dietary reference  intakes (DRI)17 (Institute of  Medicine of  the National Academies, 2002). Again, this difference  may be attributed to the tendency of  the FFQ to overestimate food  consumption (Hankins et al., 1970). Or if 80% of  the children are above the 75th percentile for  weight, then over consumption of energy may be a problem. The dental health status and dental health behaviors of  the children were assessed by a questionnaire and clinical dental exam. The children in the study had patterns of  dental visits similar to their parents with half  visiting the dentist at least once per year (54.8% and 50.5% respectively; Table 8). About two-thirds or 66.3% of  parents reported brushing their child's teeth daily. However, only 39.8% of  parents reported that they felt  their child's teeth were clean following  brushing (Table 8). Quality of  oral hygiene in young children is 1 7 According to the DRI, boys between the ages of  3-5 with low physical activity levels should have a total energy expenditure between 1,324 to 1,466 kcal/day, while girls of  the same age and physical activity level should have a total energy expenditure between 1,243 to 1,379 kcal/day. . usually assessed by parental self-reports  of  brushing. To our knowledge, no previous study has actually asked parents to give an subjective assessment of  tooth cleanliness. Only 4 out of  10 parents felt  their brushing was effective. Moreover, since fluoride  is well-recognized for  its role in the prevention of  dental caries, it was surprising that 26.1% of  the children in the study did not use fluoridated toothpaste (Table 8). With non-fluoridated  toothpaste being more challenging to find  and more expensive to purchase, it was astonishing to find  that over a quarter of  our families, many of  whom were low-income, used toothpaste without fluoride.  This finding  may be due to the concern some parents had regarding the safe  use of  fluoride  for  young children. 5.3. Early Childhood Caries (ECC) 5.3.1. Definition  and Prevalence The criteria for  caries severity in children that we used in this study are actually quite similar to the definition  of  early childhood caries (ECC) and severe early childhood caries (S-ECC) of  the American Academy of  Pediatric Dentistry (AAPD, 2003). The AAPD defines  ECC as the presence of  any decayed, missing (due to decay) or filled  primary tooth surface  (dmfs).  This definition  is equivalent to our definition  of  "dmfs  +" and "dmfs  - " criteria. S-ECC (severe ECC) is defined  by the AAPD as any smooth surface  caries on a child under 3 years of  age, or a dmfs  of  > 4 (age 3 years), >5 (age 4 years), and >6 (age 5 years). Our study used a more conservative definition  of  dmfs  < 5 as "low caries" and dmfs >5 as "high caries" for  all the children. Extending the AAPD definition  to our study sample, 62 (64.6%) children have ECC and 47 (47.5%) have S-ECC. A previous study of  low-incomeVietnamese children ages 3 to 74 months in Vancouver reported a prevalence of  ECC of  20.5% in children over 18 months (Harrison et al., 1997). Assessments of  children entering kindergarten in Vancouver concluded 27.4% had nursing bottle tooth decay (Bassett, McDonald, & Woods, 1999). Unfortunately,  comparisons with our results are difficult  because of  the differences  in definitions  of  ECC. Certainly, the children in our study had high levels of  dental caries. 5.3.2. Explanatory Variables and Caries The bi-variate analysis demonstrated age to be significantly  related to caries experience for  children (p<0.001; Table 10). As children and their teeth age, there are increasing opportunities for  caries to develop as a result of  increased exposure to cariogenic factors. Gender also appeared to be significantly  related to caries, with girls less likely to be in the high caries group (Table 10). This significant  difference  in caries status between genders is supported by some studies on children under 6 years of  age that found  caries to be more prevalent in males (Verrips, Frencken, Kalsbeek, ter Horst, Filedt Kok-Weimar, 1992; Maciel, Marcenes, Watt, Sheiman, 2001). However, other investigators found  no gender differences  (Al-Hosani and Rugg-Gunn, 1998; Habibian, Beighton, Stevenson, Lawson, & Roberts, 2002). Moreover, our multivariate analysis demonstrated no relationship between gender and caries; only age and food  security remained as predictors of  caries severity (Table 11). In addition to age, the relationship between total household income and caries status was also statistically significant  (p=0.05; Table 10). Similar to other studies on ECC (Demers et al., 1990; Litt et al., 1995; Henry, 1997), children from  families  with greater financial challenge were also more likely to have severe caries. This association may be related to accessibility to information  on prevention and dental care. Affordability  of  homecare aids such as toothbrushes as well as financial  and other stresses experienced by the parents may also be related to their children's poor oral health status (Litt et al., 1995; Quinonez et al., 2001; Ramos-Gomez et al., 2002). The multivariate analysis did not demonstrate a relationship between income and severity of  caries. However, the income variable used in the logistic regression was divided into three categories18, rather than the "collapsed" two categories used in the follow-up  bi-variate analysis (Table 10) which may explain the lack of  relationship. We also examined a variable referred  to as "food  security", i.e. whether financial concern affected  the quality or variety of  foods  the family  eats. Children from  families where food  security was a concern were also more likely to have ECC (p-0.03; Tables 10 and 11). A recent study by Casey et al (2004) demonstrated a relationship between food security and maternal depression. Both ECC and maternal depression are conditions more likely to be found  in low-income families.  Furthermore, some studies have found  food security and normal child health and development are inversely related (Alaimo, Olson, Frongillo, Briefel,  2001; Alaimo, Olson, Frongillo, 2001). Food security remained in the logistic regression as a predictor of  caries severity. Caution in interpreting the significance of  the food  security variable is necessary because of  the concern about the accuracy of  the SQ used to collect data on the variable. 1 8 In the initial multivariate analysis, the income variable was divided into three categories: less than $20,000, $20,000-$50,000, and more than $50,000. The children's z-scores for  height and weight for  their age, as well as their weight-for-stature were not significantly  related to caries status. This observation differs  from  the findings  of  Li, Navia, & Bian (1996), who reported that low height for  age was related to caries status in young children. Given the ethnic diversity amongst the children in the study, it is difficult  to know whether our z-score comparisons of  height-, weight-for-age, and weight-for-stature  based on the CDC growth chart were accurate for  our multi-ethnic children. Sugar consumption was significantly  related to caries status in this group of  children. The term "sugar" varies in ECC research from  its use as a general and undefined  term (Tinanoff  & Palmer, 2000), to a more generic term encompassing sucrose, fructose, glucose, and lactose (The National Academy of  Sciences, 2002). Although the general use of  the term "sugar" poses a challenge for  interpreting results, investigators agreed that "sugar" is associated with dental caries (Mattila et al., 2000; Tinanoff  & Palmer, 2003). The FFQ and ESHA Food Processor Program allowed for  a unique and detailed analysis of the children's sources of  dietary sugar. This in depth investigation revealed that ECC risk related to sugar consumption was different  amongst the younger and older children in the study. Similar to a study by Karjalamen, Soderling, Sewon, Lapinleimu, & Simell (2001), the percentage of  daily total sugar intake (including natural sugars from  fruits) 19 from  fluids (including milk) and snacks compared to was related to caries status for  the older children (Table 13). However, in younger children, the percentage of  daily calories contributed by 1 9 The cut-off  of  50% was used in this assessment because only one child had sugar from  fluids  and sugary snacks account for  less than 25% of  total daily sugar consumption (12 children had less than 50%). sugar was associated with caries experience (Table 12). Although we are uncertain what accounts for  the difference  in the association between sugar consumption and caries experience, we speculate it may reflect  subtle differences  in dietary practices between the younger and older children. Further, investigators have suggested that regular soft  drinks and beverages from powder are more strongly associated with caries risk than juice (Marshall et al., 2003). Unfortunately,  this could not be confirmed  in our study because of  the small number of children who reported consuming soft  drinks. Furthermore, the nature of  the data entry used in our study did not enable an analysis of  the frequency  of  foods  consumed through the day at this time. The role of  milk sugar, "lactose", remains controversial in studies of  ECC. While some studies found  evidence that suggests milk sugar may prevent caries (van Loveren & Duggal, 2001; Imfeld,  1983) or is neutral (Marshall et al., 2003), the results of  our study showed that milk consumption is related to ECC. Older children who drank less milk (< 3 cups) were more likely to be caries-free  (Table 13). However, how the milk is consumed was not investigated in our study. The cariogenicity of  milk can differ  greatly if  it is consumed during a meal compared to during sleep (Douglass, Tinanoff,  Tang, Altmen, 2001). Milk's cariogenicity is also affected  by the addition of  sweetened substances (Imfeld,  1983; van Loveren & Duggal, 2001; Tinanoff  et al., 2002). Further, when milk sugar was not included in our calculation of  sugar consumption as suggested by The National Academy of  Sciences (2002) on dietary reference  intakes for  macronutrients, total 2 0 The cut-off  of  30% was used in this assessment to provide for  some leeway for  the RDI of  25% for  sugar consumption in proportion to total daily caloric intake (The National Academy of  Sciences, 2002). sugar intake was much lower and not significantly  associated with caries status. Moreover, it is possible that children who drank less milk consumed other nutritious and less cariogenic foods  that require chewing while those children who consumed greater amounts of  milk may be displacing other foods.  Investigators have reported a decrease in milk consumption and increase in juice and soft  drink consumption in children (Borrud, Enns, Mickle, 1997). In addition to its association with dental caries, these changes in children's beverage consumption also decrease calcium intake and increases the potential for  obesity (Marshall et al., 2003). The dietary and feeding  patterns amongst these children who consumed large amounts of  milk should be examined further  for  factors  related to ECC that may differ  from  other children. Dental visits and oral health practices were assessed in the dental questionnaire and clinical exam. Children who had dental visits at least once a year (76.7%) were more likely to have a high dmfs  score than their peers who did not go to the dentist regularly (p=0.003; Table 10). Of  the 31 children with a dmfs>5,  almost one-third (29%; n=9) had full coverage crowns or teeth extracted due to decay, events which substantially increased their dmfs  score. Also included amongst the 99 children in the study are 12 children (12%) who had undergone general anesthetic for  the treatment of  caries. Stainless steel crowns are often  the treatment choice for  high-risk children who have a general anesthetic for  dental treatment. Therefore,  amongst the children who visited the dentist at least once a year were those who received extensive restorative and surgical treatment for  caries. Such comprehensive treatment would substantially increase the "m" and "f'  component of  dmfs. The use of  fluoride  as part of  regular homecare was also assessed. While 75.0% of children used fluoride  toothpaste regularly, no significant  relationship was found  between fluoride  use and caries status. This finding  does not agree with that of  other studies (Aaltonen, 1991; Health Education Authority, 1996; Sutcliff,  1996; Lopez Del Valle, Velazquez-Quintana, Weinstein, Domoto, Leroux, 1998). In addition to its positive effects in caries prevention, fluoridated  toothpaste is also more accessible and economical than non-fluoridated  toothpastes, factors  that are likely important for  parents who expressed financial  concerns. Multi-variate analysis showed dental practices and caries status were not significantly  associated in this group of  children (Table 11). 5.4. Iron Deficiency  (ID) 5.4.1. Prevalence of  Iron Deficiency The prevalence of  iron deficiency  in the preschool children in the study was 25.0%. Analysis of  iron status and age showed that the prevalence of  ID in children between 20-35 months was 38.2% and in the older children between ages 36 to 71 months was 17.7% (Table 14). Further, 9.5% of  the younger children and only 3.9% of  the older children had IDA. It is difficult  to determine whether the prevalence of  ID and IDA of  the children found  in our study is similar to the general population because most studies focus  on infants  and toddlers (Table 18). As expected, the older children in our study were less likely to have ID compared to the younger children as they require less dietary iron relative to the amount of  food  they consume. As well, older children tend to consume more iron-rich foods  including iron fortified  cereals. Table 18. Select Studies on Iron Deficiency  Anemia and Low Iron Store Location ® ate of  study Population , A ® e n Criteria for  Iron Status Classification  Prevalence (%) Study • • r (mos) Author (yr uf  Iron dellclericy • , . , I r ° n Lowiron . , Low iron stores deficiency , publication); anemia: . 1 stores ""••• anemia ^ ^ ^ ^ T v , . . . ^ Low-income, Ferritin <10ii2/L " Montreal 1989-1990 predominately 10-14 218 with'Hgb<l,15gfc  Ferritin <10^8^ 27 37 Caucasian orMCV<70fL Toronto Representativeiof' Zlotkin etal ullils^ general population Hgb <U0g/L with , . . , NR with the exception 8.6 - 15.2 428 ferritin  <10Lig/L or Ferritin <10ng/L 4.3 34 (1996) .Montreal; r . , „ „ C,„„ „ ~ : * ' Edmonton of  higher parental ZPP >100|ig/L education Hgb <101g/L, or Hgb <11 lg/Lwith 2 ' Einisetal Predominately or 3 indicators of ' Vancouver 1993 middle and higher 9 434 low iron (ie:: femtin  Ferritin < 1 O^ g/L income <10;igrt.,TD3C >60|imol/L, and ZPP >70[imol/mol MR: not reported, Hgb: hemoglobin, ZPP zinc protoporphyrin; 'ITBC: total iron binding capacity, MCV: mean ceil volume 7 24 5.4.2. Explanatory Variables and Iron Deficiency Age was significantly  related to iron status. Younger children, as previously described, were more likely to have ID (p=0.05; Table 14). Differences  in eating patterns between the younger and older children likely explain this difference  in iron status. Gender also approached significance  in relation to iron status (p=0.06; Table 15). Females appeared to be more likely to be iron deficient  than their male peers, but the girls were also, on average, younger than the boys in this study which may explain the difference. Although inadequate consumption of  meat, fish,  and poultry is associated with increased risk of  ID in infants  of  nine months of  age(Innis et al., 1997), no relationship between these variables and ID was observed in the children in this study from  the data analyzed. However, excess consumption of  milk (>3 cups per day) did increase the risk of  ID in younger children (p=0.03; Table 17). This association was based on results of  the SQ and was not observed in the FFQ, so caution is needed in interpreting this result (Table 17). A link between cows' milk consumption and ID in infants  under 12 months is thought to be due to the low iron content of  bovine milk, its poor bioavailability, and the potential for intestinal bleeding associated with excess milk consumption (Fomon, Zeigler, Nelson, & Edwards, 1981; Zimmerman, 2001). As well, excessive consumption of  milk may displace the children's calories from  other nutritious and iron-rich foods. Analysis of  dental health variables showed that children's dental visits were significantly related to iron status. Children with ID were less likely to visit the dentist at least once per year (p=0.01). This finding  was not unexpected as younger children are more likely to have ID. Their parents may not take them to the dentist until they are older. Because the bivariate analyses demonstrated no relationships of  significance,  more complex multivariate analyses were not explored. 5.5. Early Childhood Caries, Iron Deficiency  and Common Explanatory Variables Caries experience and iron store status were associated with age for  the children in the study. However, the associations were in opposite directions; older children had more dental decay and ID was more prevalent in younger children. This dichotomy of  the age groups is likely a result of  differences  in eating patterns; older children consume greater quantity and varieties of  foods  compared to their younger peers and are more resistant to ID. However, these dietary habits and the longer exposure of  their teeth to cariogenic factors  increase their risk of  dental caries. Although a relationship between milk and caries was demonstrated in older children, we did not confirm  a relationship between milk and iron status in younger children because a significant  relationship was only observed in the data gathered from  the SQ. This cross-sectional, exploratory study looked at the demographics, dietary patterns, and dental health factors  that may be related to ECC and iron deficiency  in a purposive volunteer sample of  99 children aged 18 to 71 months in Vancouver, British Columbia. The observed prevalence of  ECC of  64.4% and ID of  25.0% in the sample of  children was alarming and the following  associations were found: • Older children were more likely to have ECC and younger children more likely to have ID. • Economically disadvantaged children in the study were at greater risk for  ECC as reflected  in family  income and food  security concerns. • Younger children who consumed a significant  proportion of  their calories as sugar and the older children who consumed large amounts of  sugar in beverages and snacks (not including natural sources of  sugars such as fruits)  in proportion to total sugar consumption were at increased risk for  ECC. • Although a relationship between milk consumption and ECC was observed, the relationship between milk and ID could not be confirmed  as a significant relationship was observed was not observed in both the questionnaires that inquired on milk consumption. The overall goal of  this cross-sectional, exploratory study was to determine if  two of the more common conditions of  early childhood, early childhood caries and iron deficiency,  were linked by common dietary or other etiological factors.  While no consistent links were observed, the study confirmed  some existing knowledge, demonstrated some new associations, and suggested routes of  further  inquiry. 5.7. Recommendations for  Future Research Although this exploratory study did not draw definitive  conclusions about the relationship between beverage consumption, caries, and iron status, older children with decay and younger children with iron deficiency  tend to have eating patterns related to beverage consumption that differ  from  other children. Because of  the diversity in dietary habits and frequent  changes in dietary practices, studies of  young children should focus  on a limited age range. Further studies with a larger group of  children with a smaller age range should be pursued (e.g. only children under 3 years of  age). The interaction between food security, family  income, and ECC or iron deficiency  also merit additional study. While previous investigators have found  associations between family  income and ECC or iron deficiency,  the role of  food  security in these conditions requires further  investigation due to its reported association with poverty, maternal depression, and negative health and development of  children (Alaimo, Olson, Frongillo, & Briefel,  2001; Alaimo, Olson, Frongillo, 2001; Casey et al., 2004). We encourage research in the following  areas: • Future studies should include a larger sample size to increase power of  the results involving a limited age range of  younger children (e.g. ages 2-3 years). • Future research should include case control studies that compare children under 3 years of  age with ECC to their peers without ECC. Since frequency  of  food  consumption is associated with dental caries, further studies should include a 24-hour recall of  the quantity and how foods  are consumed throughout the day. Moreover, this research should include specific  information regarding the sugar content of  beverages. Development of  appropriate assessment tool should be sought to obtain accurate reports of  beverage consumption. With the significant  relationship between socioeconomic status and ECC or ID, future  studies should investigate the link between family  income, food  security, and early childhood conditions related to feeding  patterns. Chapter 6 6. REFERENCES Aaltonen, A. S. (1991). The frequency  of  mother-infant  salivary close contacts and maternal caries activity affect  caries occurrence in 4-year-old children. Proceedings of  the Finnish Dental Society. 87. 373-382. Acs, G., Lodolini, G., Kaminsky, S., Cisneros, G. J. (1992). Effect  of  nursing caries on body weight in a pediatric population. Pediatric Dentistry. 14. 302-305. Acs, G., Shulman, R., Ng, M. W., Chussid, S. (1999). The effect  of  dental rehabilitation on the body weight of  children with early childhood caries. Pediatric Dentistry. 21(2). 109-113. Alaimo, K., Olson, C. M., Frongillo, E. A., (2001). Food insufficiency,  family  income, and health in US preschool and school-age children. American Journal of  Public Health, 91, 781-786. Alaimo, K., Olson, C. M., Frongillo, E. A., Briefel,  R. R. (2001). Food insufficiency  and American school-age children's cognitive, academic, and psychosocial development. Pediatrics. 108. 44-53. Alaluusua, S., & Malmivirta, R. (1994). Early plaque accumulation~a sign for  caries risk in young children. Community Dentistry & Oral Epidemiology. 22 (5 Pt 1), 273-276. Al-Hosani, E., Rugg-Gunn, A. (1998). Combination of  low parental education attainment and high parental income related to caries experience in pre-school children in Abu-Dhabi. Community Dentistry and Oral Epidemiology. 26. 31-36. American Academy of  Pediatric Dentistry (2003). Definition  of  early childhood caries (ECC). Pediatric Dentistry, 25(7), 9. Antrim, A. (2004, February). Iron metabolism, iron deficiency,  prevention and treatment of anemia in infants  and children. Paper presented at a Post-graduate review for  family physicians, Faculty of  Medicine, Vancouver, BC. Association of  Dental Surgeons of  British Columbia. (2001). Children's Dentistry Task Force Report. Vancouver, BC: Children's Dentistry Task Force. Baynes, R. D. & Bothwell, T. H. (1990). Iron deficiency. Annual review in Nutrition, 10, 133-148. Berkowitz, R. J. (2003). Causes, treatment and prevention of  ECC: a microbiologic Perspective. Journal of  Canadian Dental Association, 69 (5), 304-307. Berkowitz, R. (1996). Etiology of  Nursing Caries: A microbiological perspective. Journal of  Public Health Dentistry. 56 (1), 51-54. Berkowitz, R. J., Jordan, H. V., & White, G. (1975). The early establishment of Streptococcus mutans in the mouths of  infants.  Archives of  Oral Biology. 20 (3), 171-174. Borrud, L., Enns, C. W., Mickle, S. (1997). What we eat: USDA surveys food  consumption changes. Community Nutrition Institution. 27. 4-5. Bowen, W. H., Amsbaugh, S. M., Monell-Torrens, S., & Brunelle, J. (1983). Effects  of varying intervals between meals on dental caries in rats. Caries Research, 17 (5), 466-471. Brossen, E., & Stecksen-Blicks, C. (1998). Risk factors  for  dental caries in 2-year-old children. Swedish Dental Journal, 22 (1-2), 9-14. Brown, L. R., Driezen, S., & Handler, S. (1976). Effects  of  selected caries preventive regimens on microbial changes following  irradiation-induced xerostomia in cancer patients. In H. M. Stiles, W. J. Loesche, T. C. O'Brien (Eds.). Microbial aspects of  dental caries (Vol. 1). London: Information  Retrieval, 275-290. Buchanan, G. R. (1999). The tragedy of  iron deficiency  during infancy  and early childhood. Journal of  Pediatrics. 135 (4), 413-415. Burt, B. A., & Eklund, S. A. (1999). Dentistry, Dental Practice, and the Community (5th ed.). Philadelphia: WB Saunders Company. Canadian Food Guide (2004). Canada's Food Guide to Healthy Eating Focus on Preschoolers - Background for  Educators and Communicators. Available: http://www.hc-sc.gc.ca/hpfb-dgpsa/onpp-bppn/food  guide preschoolers e.html#2. Accessed: August 9, 2004. Canadian Task Force on the Periodic Health Examination (1994). Canadian Guide to Clinical Preventive Health Care. Ottawa: Health Canada. Canadian Task Force on the Periodic Health Examination (1979). The periodic health examination. Canadian Medical Association Journal, 121, 1193. Carley, A. (2003). Anemia: When is it iron deficiency? Pediatric Nursing, 39 (2), 127-133. Casey, P., Goolsby, S., Berkowitz, C., Frank, D., Cook, J., Cutts, D., Black, M., Zaldivar, N., Levenson, S., Heeren, T., Meyers, A., & the Children's Sentinel Nutritional Assessment Program Study Group (2004). Maternal depression, changing public assistance, food security, and child health status. Pediatrics. 113 (2), 298-304. Caufield,  P. W., Cutter, G. R., & Dasanayake, A. P. (1993). Initial acquisition of  mutans streptococci by infants:  Evidence for  a discrete window of  infectivity.  Journal of  Dental Research. 72. 37-45. Centers for  Disease Control and Prevention (Press Release). Community Water Fluoridation Now Reaches Two-thirds of  U.S. Population on Public Water Systems. Centers for  Disease Control and Prevention (CDCP) (1994, September). Conference, Atlanta, Georgia. Centers for  Disease Control and Prevention (1999). Water Fluoridation and Costs of Medicaid Treatment for  Dental Decay - Louisiana, 1995-1996. MMWR, 48(34), 753-757. Available:http://www.cdc.gov/mmwr/preview/mmwrhtml/mm4834a2.htm. Accessed: April 26, 2004. Centers for  Disease Control and Prevention (CDC) (2000). CDC Growth Charts: United States. Hyattsville, MD: National Center for  Health Statistics. Web site: http://www.cdc.gov/growthcharts/. Accessed: April 26, 2004. Centers for  Disease Control and Prevention (CDC) (2001). Community Water Fluoridation: Surgeon General's Statement. Web site: http://www.cdc.gov/OralHealth/factsheets/fl-surgeon2001.htm. Accessed: April 26, 2004. Centers for  Disease Control and Prevention (2001). Recommendations for  Using Fluoride to Prevent and Control Dental Caries in the United States. MMWR, 50(RR14), 1-42. Available: http://www.cdc.gov/mmwr/preview/mmwrhtml/rr5014al.htm. Accessed: April 26,2004. Chen, M. (1996). Oral health of  disadvantaged populations. In: L. Cohen & H. Gifts  (Eds.). Disease prevention and oral health promotion. Munksgaard: Copenhagen. Conrad, M. E. (2003). Iron deficiency  anemia [On-line]. Available: http://www.emedicine.com/med/topic 1188.htm. Accessed: April 26, 2004. Dallman, P. R. (1987). Iron deficiency  and the immune response. American Journal of Clinical Nutritrion. 46. 329. Dallman, P. R., Yip, R., & Johnson, C. (1984). Prevalence and causes of  anemia in the United States. American Journal of  Clinical Nutrition, 39 (3), 437-445. Davidsson, L., Galan, P., Kastenmayer, P., Cherouvrier, F., Juillerat, M. A., Hercberg, S., & Hurrell, R.F. (1994). Iron bioavailability studied in infants:  the influence  of  phytic acid and ascorbic acid in infant  formulas  based on soy isolate. Pediatric Research, 36 (6), 816-822. Davies, G. N. (1998). Early childhood caries - A synopsis. Community Dentistry and Oral Epidemiology, 26 (Suppl. 1), 106-116. Davis, J. R. & Stegeman, C. A. (1998). The dental hygienist's guide to nutritional care. Philadelphia: W.B. Saunders. DeMaeyer, E. M. (1989). Preventing and controlling iron deficiency  anaemia through primary health care. A guide for  health administrators and programme managers. Geneva, World Health Organization. Demers, M., Brodeur, J. M., Simard, P. L., Mouton, C., Veilleux, G., & Frechette, S. (1990). Caries predictors suitable for  mass-screening in children: A literature review. Community Dental Health, 7, 11-21. Dobbing, J. (1990). Vulnerable periods in developing brain. In J. Dobbing (Ed.), Brain, behavior, and iron in the infant  diet (pp. 1-7). London: Springer-Verlag. Douglass, J. M. (2000). Response to Tinanoff  and Palmer: Dietary determinants of  dental caries and dietary recommendations for  preschool children. Journal of  Public Health Dentristrv. 60 (3), 207-209. Douglass, J. M., Tinanoff,  N., Tang, J. M. W., Altman, D. S. (2001). Dental caries patterns and oral health behavious in Arizona infants  and toddlers. Community Dentistry and Oral Epidemiology, 29. 14-22. Elkman, A. (1990). Dental caries and related factors  - a longitudinal study of  Finnish immigrant children in the north of  Sweden. Swedish Dental Journal, 14, 93-99. Eurodiet core report (2001). Nutrition and diet for  healthy lifestyles  in Europe: science and policy implications [Special issue]. Public Health Nutrition, 4. Falco, M. A. (2001). The lifetime  impact of  sugar excess and nutrient depletion on oral health. General Dentistry, 49 (6), 591-595. Fairbanks, V. F. (1994). Iron in medicine and nutrition. In: M. E. Shils, J. A. Olson, M. Shike, & A. C. Ross (Eds.). Modern Nutrition in Health and Disease. Philadephia: Lea & Febiger. Fass, E. N. (1962). Is bottle feeding  of  milk a factor  in dental caries? Journal of  Dentistry for  Children. 29, 245-251. Febres, C., Echeverri, E. A., & Keene, H. J. (1997). Parental awareness, habits, and social factors  and their relationship to baby bottle tooth decay. Pediatric Dentistry, 19 (1), 22-27. Florida State University College of  Medicine (2004). Diseases of  Iron Metabolism. The Internet Pathology Laboratory for  Medical Education. Available: http://medlib.med.utah.edu/WebPath/TUTORIAL/IRON/IRON.html . Accessed April 26. 2004. Fomon, S. J., Zeigler, E. E., Nelson, S. E., & Edwards, B. B. (1981). Cow's milk feeding  in infancy:  Gastrointestinal loss and nutritional status. Journal of  Pediatratics. 98. 540-545. Gahnberg, L., Smith, D. J., Taubman, M. A., Ebersole, J. L. (1985). Salivary IgA antibody to glucosyltransferase  of  oral microbial origin in children. Archives in Oral Biology, 30, 551-556. Gary-Donald, K., Di-Tommaso, S., Leamann, F. (1990). The prevalence of  iron-deficiency anaemia in low-income Montreal infants  aged 10-14 months. Journal of  Canadian Dietetics Association, 51, 424A. Geaghan, S. M. (1999). Hematologic values and appearance in the healthy fetus,  neonate, and child. Clinics in Laboratory Medicine. 19 (1), 1-37. Gleeson, M., Dobson, A. J., Firman, D. W., Cripps, A. W., Clancy, R. L., Wlodarczyk, J. H., Hensley, M. J. (1991). The variability of  immunoglobins and albumin in salivary secretions of  children. Scandinavian Journal of  Immunology, 33, 533-541. Gibson, R. S. (1990). Principles of  nutritional assessment. New York: Oxford  University Press. Greene-Firestone, L., Feldman, W., & Luke, B. (1991). Prevalence and risk factors  of  iron depletion and iron deficiency  anemia among infants  in Ottawa-Carlton. Journal of Canadian Dietetic Association, 52, 20-33. Grindefjord,  M., Dahllof,  G., Nilsson, B., & Modeer, T. (1995). Prediction of  dental caries development in 1-year-old children. Caries Research, 29 (5), 343-348. Grindulis, H., Scott, P. H., Belton, N. R., & Wharton, B. A. (1986). Combined deficiency of  iron and vitamin D in Asian toddlers. Archives of  Diseases in Childhood, 61, 843-848. Grytten, J., Ingeborg, R., Hoist, D., & Steele, L. (1988). Longitudinal study of  dental health behaviors and other caries predictors in early childhood. Dental health behavior among infants.  16. 356-359. Gustafsson,  B. E., Quesnsel, C. E., Swenander-Lanke, L., Lundqvist, C., Grahnen, H., Bonow, B.E., & Krasse, B. (1954). The Vipeholm dental caries study. The effect  of different  levels of  carbohydrate intake on caries activity in 436 individuals observed for five  years. Acta Odontologica Scandinavia. 11, 232-236. Habibian, M., Beighton, D., Stevenson, R., Lawson, M., Roberts, G. (2002). Relationships between dietary behaviours, oral hygiene and mutans streptococci in dental plaque of  a group of  infants  in Southern England. Archives of  Oral Biology, 47, 491-498. Hallberg, L., & Rossander, L. (1984). Improvement of  iron nutrition in developing countries: comparison of  adding meat, soy protein, ascorbic acid, citric acid, and ferrous sulphate on iron absorption from  a simple Latin American-type of  meal. American Journal of  Clinical Nutrition. 39 (4), 577-583. Hankin, J. H., Messinger, H. B., & Stallones, R. A. (1970). A short dietary method for epidemiological studies. IV: Evaluation of  questionnaire. American Journal of Epidemiology. 91. 562-567. Harrison, R., Wong, T., Ewan, C., Contreras, B., & Phung, Y. (1997). Feeding practices and dental caries in an urban Canadian population of  Vietnamese preschool children. Journal of  Dentistry for  Children. 64 (2). 112-117. Health Education Authority (1996). The scientific  basis of  dental health education: A policy document (4th ed.). London: Health Education Authority. Health and Welfare  Canada (1990). Scientific  Review Committee: Nutrition recommendations, Ottawa. Canada. Henry, R. J. (1997). Why do 20% of  our children experience 80% of  the decay? An update on the status of  childhood caries. Texas Dental Journal, 114 (1), 10-14. Holbrook, W. P., de Soet, J. J., & de Graaff,  J. (1993). Prediction of  dental caries in pre-school children. Caries Research, 27,424-430. Horowitz, H.S. (1998). Research issues in early childhood caries. Community Dentistry and Oral Epidemiology, 26 (Suppl. 1), 67-81. Hurrell, R. F. (1997). Bioavailability of  iron. European Journal of  Clinical Nutrition, 51 (Suppl. 1), 4-8. Hurtado, E. K., Claussen, A. H., & Scott, K. C. (1999). Early childhood and mild or moderate mental retardation. American Journal of  Clinical Nutrition, 69, 115-119. Imfeld,  T. (1983). Identification  of  low-risk dietary components. New York: Karger. Innis, S. M., Nelson, C. M., Wadsworth, L. D., MacLaren, I. A., & Lwanga, D. (1997). Incidence of  iron-deficiency  anemia and depleted iron stores among nine-month-old infants in Vancouver, Canada. Canadian Journal of  Public Health, 88, 80-84. Johnsen, D. C. (1982). Characteristics and backgrounds of  children with "nursing caries". Pediatric Dentistry. 4. 218-224. Karjalamen, S., Soderling, E., Sewon, L., Lapinleimu, H., Simell, O. (2001). A Prospective study on sucrose consumption, visible plaque and caries in children from  3 to 6 years of age. Community Dentistry and Oral Epidemiology, 29, 136-142. Kawabata, K., Kawamura, M., Sasahara, H., Morishita, M., Bachchu, M. A., & Iwamoto, Y. (1997). Development of  an oral health indicator in infants. Community Dental Health, 14.(2), 79-83. Keyes, P. H., & Jordan, H. V. (1963). Factors influencing  the initial transmission and inhibition of  dental caries. In: R. S. Harris (Ed.). Mechanisms of  hard tissue destruction. New York: NY Academic Press, 261-283. Khan, M. N., & Cleaton-Jones, P. E. (1998). Dental caries in African  preschool children. Social factors  as disease markers. Journal of  Public Health Dentistry, 58. 7-11. Klock, B. & Krasse, B. (1979). A comparison between different  methods fro  prediction of caries activity. Scandinavian Journal of  Dental Research, 87,129-139. Kotlow, L. A. (1977). Breast feeding:  A cause of  dental caries in children. Journal of Dentistry for  Children, 25. 192-193. Krausse, B. (1965). The effect  of  caries inducing streptococci in hamsters fed  diets with sucrose or glucose. Archives of  Oral Biology, 10, 223-226. Lee, R. D. & Nieman, D. C. (2003). Nutritional Assessment (3rd ed.). Toronto: Mosby. Lehmann, F., Gray-Donald, K., Mongeon, M., & Di Tommaso, S. (1992). Iron deficiency anemia in 1-year-old children of  disadvantaged families  in Montreal. Canadian Medical Association Journal, 146, 1572-1577. Lesperance, L., Wu, A. C., & Bernstein, H. (2002). Putting a dent in iron deficiency. Contemporary Pediatrics. 19 (7), 60-79. Leverett, D. H., Featherstone, J. D., Proskin, H. M., Adair, S. M., Eisenberg, A. D., Mundorff-Shrestha,  S. A., Shields, C. P., Shaffer,  C. L., & Billings, R. J. (1993). Caries risk assessment by a cross-sectional discrimination study. Journal of  Dental Research, 72, 529-537. Levitsky, D. A. & Strupp, B. J. (1995). Malnutrition and the brain: changing concepts, changing concerns. Journal of  Nutrition. 125 (Suppl. 8), 2212-2220. Levy, S. M. (2003). An update on Fluorides and Fluorosis. Journal of  Canadian Dentistry Association, 69 (5), 286-291. Levy, S. M., Warren, J. J., Broffitt,  B., Hillis, S. L., and Kanellis, M. J. (2003). Fluoride, beverages and dental caries in the primary dentition. Caries Research, 37, 157-165. Litt, M. D., Reisine, S., & Tinanoff,  N. (1995). Multidimensional causal model of  dental caries development in low-income preschool children. Public Health Reports, 110, 607-617. Looker, A. C., Dallman, P.R., Carroll, M. D., Gunter, E.W., & Johnson, C. L. (1997). Prevalence of  iron deficiency  in the United States. JAMA. 277. 973-976. Lopez Del Valle, L., Velazquez-Quintana, Y., Weinstein, P., Domoto, P., Leroux, B. (1998). Early childhood caries and risk factors  in rural Puerto Rican children. ASDC Journal of  Dentistry for  Children, 65, 132-135. Losnedahl, K. J., Wang, H., Aslam, M., Zou, S., Hurley, W. L. (1996). Antimicrobial factors  in milk [On-line]. Available: http ://www.aces .uiuc. edu/~ansvstem/ dairyrep96/Losnedahl. html .Accessed April 20^2004. Low, W., Tan, S., Schwartz, S. (1999). The effect  of  severe caries on the quality of  life  in young children. Pediatric Dentistry, 21, 325-326. Lozoff,  B., Brittenham, G. M., Wolf,  A. W., McClish, D. K., Kuhnert, P. M., Jimenez, E., Jimenez, R., Mora, L. A., Gomez, I., & Krauskoph, D. (1987). Iron-deficiency  anemia and iron therapy: effects  on infant  developmental test performance. Pediatrics, 79, 981-985. Lozoff,  B., Brittenham, Wolf,  A. W., & Jimenez, E. (1996). Iron-deficiency  anemia and infant  development: Effects  of  extended oral iron therapy. Journal of  Pediatrics, 129, 382-389. Lozoff,  B., Jimenez, E., Hagen, J., Mollen, E., & Wolf,  A. (2000). Poorer behavioral and developmental outcome more than 10 years after  treatment for  iron deficiency  in infancy. Pediatrics, 105(4). E51. Lozoff,  B., Jimenez, E., & Wolf,  A. W. (1991). Long-term developmental outcome of infants  with iron deficiency. New England Journal of  Medicine, 325, 687-694. Lozoff,  B., Klein, N. K., Nelson, E. C., McClish, Manuel, M„ & Chcon, M. E. (1998). Behavior of  infants  with iron-deficiency  anemia. Child Development, 69, 24-36. Lwanga, D. (1996). Iron status of  infants  of  9 months of  age in Vancouver, B.C. Unpublished M.Sc. Thesis, University of  British Columbia. Maciel, S. M., Marcenes, W., Watt, R. G., Sheiham, A (2001). The relationsip between sweetness preference  and dental caries in mother/child pairs from  Maringa-Pr. Brazil. International Dental Journal, 51, 83-88. Marshall, T. A., Levy, S. M., Broffitt,  B., Warren, J. J., Eichenberger-Gilmore, J. M., Burns, T. L., Stumbo, P.J. (2003). Dental caries and beverage consumption on young children. Pediatrics. 112(3), e 184-e 191. Mattila, M. L., Paunio, P., Rautava, P., Ojanlatva, A., Sillanpaa, M. (1998). Changes in dental health habits from  3 to 5 years of  age. Journal of  Public Health Dentistry, 58, 270-274. Mattila, M. L., Rautava, P., Sillanpaa, M. & Paunio, P. (2000). Caries in five-year-old children and associations with family-related  factors. Journal of  Dental Research, 79 (3), 875-881. McGhee, J. R. & Kiyono, H. (1993). New perspectives in vaccine development: mucosal immunity to infections. Infectious  Agents & Disease, 2 (2), 55-73. Messer, L. B. (2000). Assessing caries risk in children. Australian Dental Journal, 45 (1), 10-16. Michaelsen, K. F., Weaver, L., Branca, F., & Robertson, A. (2000). Feeding and nutrition of  infants  and young children: Guidelines for  the WHO European Region with emphasis on the former  Soviet countries. Denmark: WHO. Michalek, S. M. & Childers, N. K. (1990). Development and outlook for  a caries vaccine. Critical Review of  Oral Biological Medicine, 1, 37-54. Mikkelsen, L. (1996). Effect  of  sucrose intake on numbers of  bacteria in plaque expressing extracellular carbohydrate metabolizing enxymes. Caries Research, 30, 65-70. Moffatt,  M. E. K., Longstaffe,  S., Besant, J., & Dureski, C. (1994). Prevention of  iron deficiency  and psychomotor decline in high-risk infants  through use of  iron fortified  infant formula. Journal of  Pediatrics, 125, 527-534. National Institutes of  Health (1996). The national survey of  dental caries in U.S. children. Washington, D.C.: Government Printing Office. Newbrun, E. (1989). Effectiveness  of  water fluoridation  [Special issue]. Journal of  Public Health Dentistry, 49, 279-89. Oski, F. A. (1993). Iron deficiency  in infancy  and childhood. New England Journal of Medicine, 329, 190-193. Parks, Y. A. & Wharton, B. A. (1989). Iron deficiency  and the brain. Acta Paediatrica Scandinavica, 361, (Suppl.), 71-77. Paunio, P., Rautava, P., Helenius, H., Alanen, P., & Sillanpaa, M. (1993). The Finnish Family Competence Study: the relationship between caries, dental health habits and general health in 3-year-old Finnish children. Caries Research, 27 (2), 154-160. Petersen, P. E. (1992). Oral health behaviour of  6-year-old Danish children. Acta Odontologica Scandinavia. 50, 57-64. Pitts, N. B. (1997). Patient caries status in the context of  practical, evidence-based management of  the intial caries lesion. Journal of  Dental Education, 61 (11), 861-865. Poulsen, S., Agerbaek, N., Melsen, B., Korts, D. C., Glavind, L., & Rolla, G. (1976). The effect  of  professional  toothcleansing on gingivitis and dental caries in children after  1 year. Community Dentistry & Oral Epidemiology, 4(5), 195-199. Quinonez, R. B., Keels, M. A., Vann Jr, W. F., Mclver, F. T., Heller, K., Whitt, J. K. (2001). Early childhood caries: Analysis of  psychosocial and biological factors  in a high-risk population. Caries Research, 35, 376-383. Ramos-Gomez, F. J., Weintraub, J. A., Gansky, S. A., Hoover, C. I., & Featherstone, J. D. (2002). Bacterial, behavioral and environmental factors  associated with early childhood caries. Journal of  Clinical Pediatric Dentistry, 26 (2), 165-173. Reisine, S., & Douglass, J. M. (1998). Psychosocial and behavioral issues in early childhood caries. Community Dentistry and Oral Epidemiology, 26 (Suppl. 1), 32-44. Reynolds, E. C. & Wong, A. (1983). Effect  of  absorbed protein on hydroxyapatite zeta potential and streptococci  mutans adherence. Infection  and Immunity, 39, 1285-1290. Rugg-Gunn, A. J. (1996). Diet and dental caries. In J. J. Murray (Ed.): Prevention of  Oral Disease. Oxford:  Oxford  University Press, 3-31. Saarinen, U. M. (1978). Need for  iron supplementation in infants  on prolonged breastfeeding. Journal of  Pediatrics. 93, 177-180. Saarinen, U. M., Siimes, M. A., & Dallman, P. R. (1977). Iron absorption in infants:  high bioavailability of  breast milk iron as indicated by the extrinsic tag method of  iron absorption and by the concentration of  serum ferritin. Journal of  Pediatrics, 91 (1), 36-39. Sargent, J. D., Stukel, T. A., Dalton, M. A., Freeman, J. L., & Brown, M. J. (1996). Iron deficiency  in Massachusetts communities: Socioeconomic and demographic risk factors among children. American Journal of  Public Health, 86. 544-550. Serwint, J. R., Mungo, R., Negrete, V. F., Duggan, A. K., & Korsch, B.M. (1993). Child-rearing practices and nursing caries. Pediatrics, 92 (2), 233-237. Seow, W. K. (1998). Biological mechanisms of  early childhood caries. Community Dentistry and Oral Epidemiology, 26 (1), 8-27. Seow, W. K., Amaratunge, A., Sim, R., Wan, A. (1999). Prevalence of  caries in urban Australian aborigines aged 1-3.5 years. Pediatric Dentistry, 21, 91-96. Shah, M., Griffin,  I. J., Lifschitz,  C. H., & Abrams, S. A. (2003). Effect  of  orange and apple juices on iron absorption in children. Archives of  Pediatrics & Adolescent Medicine, 157. 1232-1236. Sheiham, A. (1991). Why free  sugars consumption should be below 15kg per person per year in industrialized countries: the dental evidence. British Dental Journal, 171, 63-65. Sheiham, A. (2001). Dietary effects  on dental disease. Public Health Nutrition. 4 (2B), 569-591. Sjogren, K., & Birkhed, D. (1993). Factors related to fluoride  retention after  tooth-brushing and possible connection to caries activity. Caries Research, 27, 474-477. Skinner, J. D., Carruth, B. R., Bounds, W., Ziegler, P., Reidy, K. (2002). Do food-related experiences in the first  2 years of  life  predict dietary variety in school-aged children? Journal of  Nutrition Education and Behavior, 34, 310-315. Slade, G. D., Spencer, A. J., Davies, M. J., Stewart, J., F. (1996). Influence  of  exposure to fluoridated  water on socioeconomic inequalities in children's caries experience. Community Dentistry and Oral Epidemiology, 24, 89-100. Stacey, M. A., & Wright, F. A. C. (1991). Diet and feeding  patterns in high risk pre-school children. Australian Dental Journal. 36 (6), 421-427. Statistics Canada (2001). The People: Changing Faces. Available: 006 e.htm. Accessed: August 10, 2004. Sullivan, P. B. (1993). Cows' milk induced intestinal bleeding in infancy. Archives of Disease in Childhood. 68 (2), 240-245. Sutcliff,  P. (1996). Oral cleanliness and dental caries. In: J. J. Murray (Ed.): The prevention of  oral disease. Oxford:  Oxford  University Press. Tanzer, J. M. (1989). On the changing cariogenic chemistry of  coronal plaque. Journal of Dental Research. 68. 1576-1587. Tanzer, J. M. (1992). Microbiology of  dental caries. In J. Slots & M. A. Taubman (Eds.), Contemporary Oral Microbiology and Immunology (pp. 377-424). St. Louis, Mo: Mosby. The National Academy of  Science (2000). Dietary reference  intakes for  vitamin A, vitamin K, arsenic, boron, chromium, copper, iodine, iron, manganese, molybdenum, nickel, silicon, vanadium, and . http://www.nap.edu/. Accessed on September 30, 2004. The National Academy of  Science (2002). Dietary reference  intakes for  energy, carbohydrates, fiber,  fat,  protein and amino acids (Macronutrients). Available: http://www.nap.edu/. Accessed on June 26, 2004. Tinanoff,  N. (1998). Introduction to the Early Childhood Caries Conference:  Initial description and current understanding. Community Dentistry and Oral Epidemiology, 26 (Suppl. 1), 5-7. Tinanoff,  N., & O'Sullivan, D. M. (1997). Early childhood caries: overview and recent findings. Pediatric Dentistry, 19 (1), 12-16. Tinanoff,  N., & Palmer, C. A. (2003). Dietary Determinants of  dental caries and dietary recommendations for  preschool children. Refuat  Hapeh Vehashinavim, 20, 8-23. Tinanoff,  N., Kanellis, M. J., & Vargas, C. M. (2002). Current understanding of  the epidemiology, mechanisms, and prevention of  dental caries in preschool children. Pediatric Dentistry. 24 (6), 543-551. Tsubouchi, J., Tsubouchi, M., Maynard, R. J., Domoto, P. K., & Weinstein, P. (1995). A study of  dental caries and risk factors  among Native American infants. Journal of  Dentistry for  Children. 62 (4), 283-287. US Department of  Health and Human Services (2000). New CDC growth charts provide tool to ward off  future  weight problems. Available: http://www.hhs.gOv/news/press/2000pres/20000530.html. Accessed: August 10, 2004. Valaitis, R., Hesch, R., Passarelli, C., Sheehan, D., Sinton, J. (2000). A systematic review of  the relationship between breastfeeding  and early childhood caries. Canadian Journal of Public Health, 91 (6), 411-417. van Loveren, C., & Duggal, M. S. (2001). The role of  diet in caries prevention. International Dental Journal. 51. 399-406. Vargas, C. M., Crall, J. J., & Schneider, D. A. (1998). Socio-demographic distribution of pediatric dental caries: NHANES III, 1999-1994. Journal of  American Dental Association. 129,1229-1238. Verrips, G. H., Frencken, J. E., Kalsbeek, H., ter Horst, G., Filedt Kok-Weimar, T. L. (1992). Risk indicators and potential risk factors  for  caries in 5-year-olds of  different  ethnic groups in Amsterdam. Community Dentistry and Oral Epidemiology, 20, 256-260. von Houte, J. (1980). Bacterial specificity  in the etiology of  dental caries. International Dental Journal, 30, 305-326. van Houte, J., Gibbs, G., & Butera, C. (1982). Oral flora  of  children with "nursing-bottle caries." Journal of  Dental Research, 61,382-385. Walter, T., De Andraca, I., Chadud, P., & Perales, C. G. (1989). Iron deficiency  anaemia: Adverse effects  on infant  psychomotor development. Pediatrics, 84, 7-17. Wan, A. K., Seow, W. K., Purdie, D. M., Bird, P. S., Walsh, L. J., & Tudehope, D. I. (2001). Oral colonization of  Streptococcus mutans in six-month-old predentate infants. Journal of  Dental Research. 80 (12), 2060-2065. Wardlaw, G. M. (1997). Contemporary nutrition: Issues and insights (3rd ed.). Iowa: Brown & Benchmark. Weinstein, P. (1998). Public health issues in early childhood caries. Community Dentistry and Oral Epidemiology. 26 (Suppl.l), 84-90. Weinstein, P., Domoto, P., Wohlers, K., & Koday, M. (1992). Mexican-American parents with children at risk for  baby bottle tooth decay: pilot study at a migrant farmworkers clinic. Journal of  Dentistry for  Children. 59 (5), 376-383. Wendt, L. K., Hallonsten, A. L., Koch, G., & Birkhed, D. (1994).Oral hygiene in relation to caries development and immigrant status in infants  and toddlers. Scandinavian Journal of Dental Research. 102 (5), 269-273. Williams, P. (2001). Iron status among infants  9-24 months of  age in Vancouver and socio-cultural/dietary predictors of  risk for  iron deficiency  anemia. Unpublished doctorial dissertation, University of  British Columbia, British Columbia. Winter, G. B„ Rule, D. C., Mailer, G. P., James, P. M., & Gordon, P. H. (1971). The prevalence of  dental caries in pre-school children aged 1 to 4 years. British Dental Journal 130(10). 434-436. Wu, A.C., Lesperance, L., & Bernstein, H. (2002). Screening for  iron deficiency. Pediatrics in Review, 23 (5). 171-178. Yip, R., & Dallman, P. R. (1996). Iron. In: E. E. Ziegler & L. J. Filer (Eds.), Present Knowledge in Nutrition. Washington DC: ILSI Press. Zimmermann, M. (2001). Burgerstein's handbook of  nutrition: Micronutrients in the prevention and therapy of  disease. New York: Thieme. Zlotkin, S. H., Ste-Marie, M., Kopelman, H., Jones, A., Adam, J. (1996). The prevalence of iron depletion and iron-deficiency  anaemia in a randomly selected group of  infants  from four  Canadian cities. Nutrition Research, 16(5), 729-733. Zlotkin, S. (2003). Clinical nutrition: 8. The role of  nutrition in the prevention of  iron deficiency  anemia in infants,  children and adolescents. Canadian Medical Association Journal. 168 (1). 59-63. Chapter 7 7. APPENDICES Appendix A Certificates  of  Approval Appendix B Study Team and Chronology of  Study-related Meetings Appendix C Consent Forms Appendix D Screening Questionnaire Appendix E Food Frequency Questionnaire Appendix F Oral Health Questionnaire Appendix G Anthropometrics Form Appendix H Dental Exam Appendix B: Study Team and Chronology of  Study-related Meetings Study Team Name Dr. Rosamund Harrison Dr. Gary Derkson Dr. Sheila Innis Ann Szeto Ziba Vaghri Dr. Pam Glassby Barbara Crocker Tana Wyman Sue Wastie Role Chair, Pediatric Dentistry Associate Professor,  Faculty of  Dentistry Head, Department of  Dentistry Associate Professor Director Nutrition Research Program Professor,  Department of  Pediatrics MSc Candidate, Faculty of  Dentistry PhD Candidate, Faculty of  Nutrition Supervising Dentist Instructor Community Nutritionist Dental Hygienist Speech Pathologist Organization University of  British Columbia University of  British Columbia BC Children's Hospital University of  British Columbia BC Research Institute University of  British Columbia University of  British Columbia University of  British Columbia Vancouver Community Dental Program University of  British Columbia Vancouver Coastal Health Authority Vancouver Coastal Health Authority Vancouver Coastal Health Authority Chronology of  Study-related Meetings: Date Activity Location July 2002 Meeting BC Research Institute October 1,2002 Meeting BC Research Institute Meeting with January 8,2003 Speech Language Pathologists Mt St Joseph Hospital January 14, 2003 Recruitment Food Bank Trout Lake Food Bank January 27, 2003 Meeting BC Research Institute January 28,2003 Recruitment Raven Song Community Center February 18, 2003 Meeting North Health Office February 18,2003 Recruitment Raycam Community Center February 26, 2003 Meeting North Health Office March 4, 2003 Focus Group North Health Office March 5, 2003 Meeting North Health Office March 6, 2003 Meeting North Health Office Unitarian Church & First Lutheran March 11, 2003 Recruitment Food Bank Church March 12,2003 Recruitment Food Bank Raycam Community Center March 14, 2003 Recruitment Eastside Family Place March 26,2003 Meeting with staff  & volunteers North Health Office April 30, 2003 Meeting North Health Office May 5, 2003 Dental & Nutrition Clinic North Health Office May 7,2003 Meeting BC Research Institute May 12, 2003 Dental & Nutrition Clinic North Health Office May 20, 2003 Meeting BC Research Institute May 26, 2003 Dental & Nutrition Clinic North Health Office June 2,2003 Dental & Nutrition Clinic North Health Office Appendix D: Screening Questionnaire B£> Dear parents os We need your help! We know thcrt children pan have strong likes and dislikes when it comes to choosing food and drink. We are a research team from Vancouver who are-working with Parents, Speech-Language Pathologists, Nutritionists, Dentists and Health Nurses in the community to find out what young children eat and to try to find out how the foods they choose affect their development. We would like you to be part of our research to gather information on which food children like to eat. The first thing we have to do is to collect information on a large number of pre-school children. So we are asking you to complete this survey and return it to us. Someone from our research team can help you if necessary, or you can fill it out yourself and send it back to us. There are no right or wrong answers, only answers that best describe what you feel or think. The second step of this research will involve a small number of children for measuring and weighing, a dental exam, and a blood count. There are no costs to you for these tests. Please indicate if you are willing to help in the second step of this research on the end of the form. All your responses will be strictly confidential. THANK YOU FOR YOUR HELP! Dr. Sheila Innls and Ziba Vaghri Subject Code # CHILDREN'S EATING PREFERENCES One Year to Five Years of Age Please choose the answers that best describe your child. 1. FOOD: a) Does your child eat meat, fish1 or poultry2? O No • Less than 5 times a week n 5 times a week OMore than 5 times a week b) Does your child avoid any of these foods? (check ail that apply) • Eggs • Milk • Fish/Shellfish1 • Lamb • Poultry 2 • Beet products D Pork products c) Children's intakes often vary from one day to the next. On average, how many times a day, including  all  meals,  snacks  and  treats , does your child eat something? • One • Two O Three a Four • Five dSix a Seven D Eight a Nine DTen • More than ten heck which of the following your child always or almost always eats: u Dieakfast • Lunch n Dinner 2 DRINKS: a) How many cups/bottles of milk does your child drink per day? (One cup = 250 ml = 8 oz or one standard single-serving tetra pack) • None O.Ono • Two • Three • Four • Five • More than five b) How many cups/bottles of juice does your child drink a day? • None n One • Two • Three • Four • Five • More than five c) My child drinks mostly:., (can check more than one) • Milk O whole 3.3% O 2% O 1% O skim O chocolate O goat Osoy O nee • Coffee  • Tea • Fruit juico/drink • Pop/soda • Other 3. How many times a day are your child's teeth brushed with toothpaste? • By the child O zero O one O two O three • By the parent O zero O one O two o three % Yesterday, did your child eat...? (please check all that apply) • Meat • Fish/Shellfish' • Poultry 2 • None of these 1- Includes fish, crab, lobster, oysters, clams, scallop, mussels, etc. 2- Includes: chicken, duck, turkey, etc. Subject Code # CHILDREN'S EATING PREFERENCES One Year to Five Years of Age 5. My child likes/dislikes: IJkes Dislikes Not offered Foods that require chewing (moat, chicken, etc.) • • • Soft foods (yogurt, soft fruits,  cooked vegetables) • O • Crunchy foods (raw vegetables, hard fruits,  etc.) • • • 6. Are you concerned about your child's eating? • Yes n No Why? Please check all that apply n Picky eater • Doesn't eat often enough • Won't try new foods • Eats too much • Always eats the same foods • Eats unhealthy foods • Eats too often • Not enough variety in diet • Doesn't eat enough • Other   7. Was your child breast-fed? • Yes • No For how long?  8. !Gldybur !<M Infant formula? • No n Iron-fortified  formula O Regular formula (non iron fortified) For how long? 9. Does your child take a vitamin/mineral supplement? • Yes • No Please list name of supplement^) and how often taken: 10. How often has someone In your family not eaten the quality or variety of foods that you wanted because of lack of money? • Always • Almost always • Sometimes • Hardly ever • Never 11. Please record your postal code Subject Code # CHILDREN'S EATING PREFERENCES One Year to Five Years of Age Child's Background Gender • Male • Female Date of Birth ....-..• / / Month Day Year Birth Weight Place of Birth . Child's weight (if known) (specify lbs or kg) • don't know Child's height (if known) don't know Child's waist measurement (if known) • don't know Ethnic Background Mother's Ethnicity .... Father's Ethnicity Parent's Background 1. What is the total income in your family? (i.e. yours and your partner's income) • Less than $20,000 • $20,000 - $50,000 • More than $50,000 2. Highest level of education completed (Mother) • Less than high school • High school • College How many years? • University How many years? r Degree attained (specify) (Father) • Less than high school • High school • College How many years? • University How many years? • Degree attained (specify) Subject Code # CHILDREN'S EATING PREFERENCES One Year to Five Years of Age Participation in the Second Stage The second stage of this study will involve a free dental exam and blood screening of your child. Your child's measurements will also be taken. The time commitment for this will be about 30 minutes. Blood screening will involve taking a small amount of blood. May we contact you to ask for your child's participation? By agreeing to future contact, this does not mean that you are obligated to participate. If you would like to participate in this second stage please write your name, address and phone number below and someone from cur team will contact you. • Yes/Maybe -1 would like to take part in the second stage of the research. Name - ................•,-......, . ..,. . . ..,„-.. ,.:,, Phone Number .,„...,.,-.   Address . ..:  Street number and name City Province Postal Code What time of day would be best to contact you by pnone9 • Morning • Afternoon • Evening Specify time ... . Specify time Specify time • No -1 don't want to participate in the second stage of the research. Appendix E: Food Frequency Questionnaire University of  British Columbia Ham Name Brand/Homemade ' Amount Frequency DAIRY PRODUCTS Milk (drinking) - cow (homo, 2%. 1%. skim), goat, rice, ~ r~—— • cup/ml O Day soy. chocolate, hotchocolate v .• ... , ... ... a cup/ml • Day 2) Goat's milk .. . . ..... . .... . • cup/ml • Day 3) Milk in cereal . . . . . . . . . : _ _ . U cup/ml 13 Day 4) Cheese . . • 02/g • Day - Cheddar, mozzareila, Swiss, brie • cup • Week • slice 5) Cream cheese . .. .. . Doz/g Q Day . """ O Brand Olsp • Week • Homemade OTsp O Every 2 weeks 6) Cottage cheese(1%, . .. Ooz/g .. ... . • Day 2%, creamed or whole) ' -J" • cup • Week D piece O Every 2 weeks 7) Processed cheese (Lite . • Day or regular-including the ones on O Brand O Slices • Week sandwiches and hamburgers) O Every 2 weeks 8) Cheese Spreads (Lite ... .. . . Ooz/g . O Day - and regular) Cheez Whi2 O Brand • tsp O Week - Country Crock O Tsp O Every 2 weeks 9) Soy cheese ~ Ooz/g • Day • Brand Ocup • Week • Piece O Every 2 weeks 10) Goat cheese ......... ...... • . ...... . • oz/g • Day • Piece D Week • Every 2 weeks 11) Paneer .... • oz/g . O Day QWeek • Every 2 weeks 12) Yogurt .. ., f l Brand Ooz/g • Day • cup/ml • Week • Every2 weeks 13) Minigo (Yoplait . , . ........ , Qoz/g ODay fresh cheese product) . " ' Q cup/ml • Week University of  British Columbia Item Name BrandfHomemado Amount Frequency • Every 2 weeks 14) Ico cream/ Frozen , . .. • Brand . • cup/ml • Day y°9 u r t O Week • Every 2 weeks 15); Milkshakes/ • Brand • cup/ml • Day Yogurt shakes nweek • Every 2 weeks 16); Puddings . . . . . . . .. • Brand n cup/ml DDay • Homemade ,:, • Week • Every 2 weeks 17) Other Dairy Products- j ______ Doz/g • Day eggnog, Caresses, fresh cheese • cup/ml DWeek • piece O Every 2 weeks EGGS :1) 1.99? • number O Day -"fried; scrambled DWeek - poached, deviled, boiled • Every 2 - omelet, quiches weeks • number • Day 2 ) Egj) yolk only - ~ DWeek - 1 • Every 2 weeks • • • • • - . ... . D number • Day 3 ) Egg whites only DWeek • Every 2 weeks TABLE/COOKING FAT 1) .Margarine; • Brand . Ooz/g ............... DDay for spreading on breads and crackers ©tsp. DWeek { OTsp 2) Margarine • Brand Ooz/g 0 Day for spreading on vegetables or cooking ' d tsp DWeek vegetables and eggs and... OTsp D Every 2 weeks 3) Butter D Brand Doz/g DDay for spreading on breads and crackers Dtsp DWeek D Tsp D Every 2 weeks 4). Butter • Brand Doz/g .. _. o Day for spreading on vegetables or cooking D tsp D Week vegetables and eggs and... O Tsp: O Every 2 weeks 5) Cooking oils (example . D Brand Dtsp DDay In cooking pancakes • Homemade OTsp DWeek Itcm.Name 6) Salad Dressings 7) Mayonnaise  Miracle Whip 8) Peanut butler ' - tahini. nut butters 9) Whipped Toppings - CooiWhip, Nutri Whip - whipping cream 10) Other Table/Cooking Fats - cereal cream, sour cream BREADS/CEREAtS AND BAKED GOODS »*!)•• Bread (including pita/bagels) com, rye, soyrdough, chapatti, roli 2). Buns/Rolls ........ ...,,..... (including hamburger/hot dog buns) 3) Breadsticks/Croutons , 4); Cereals, cold breakfast 5) Cereals, hot breakfast 6) Wheat germ (used in/on foods) 7) PancakesAW affles 8) Muffins,  bran, fruit 9) English Muffin Brand/Homemade University of  British Colu mbia Amount = Frequency • Every 2 weeks D Brand • Brand O Brand • Homemade D Brand D Homemade • tsp O Tsp • cup/ml • oz/g C tsp • Tsp • oz/g • tsp • Tsp O oz/g • tsp • Tsp .••tsp • Tsp • cup/ml • Day • Week • Every 2 weeks n Day • Week • Every 2 weeks • Day • Week • Every 2 weeks • Day • Week D Every 2 weeks • Day • Week • Every 2 weeks _. • piece • Day • Brand " DWeek • Homemade -:•.••'•. • piece • Day D Brand - . ' ia Week P Homemade : •• • piece . . • Day • Brand • Week • Homemade . • cup • Day D Brand _ DWeek • Homemade • cup • Day • Brand • Week • Homemade - • tsp • Day • Brand DTsp DWeek D Homemade • Every 2 weeks a piece DDay • Brand *" DWeek • Homemade • Every 2 weeks • p ece O Day • small DWeek • iatge • Every 2 weeks ......... H«m Name 10) Sconss/Tea Biscuits ToasterPastries 12) Oonult/Frifers 13) Danish/Pastries 14) Croissants 15) Cakes/Squares - brownies, cake roils, 17) Cookies 18) TortHte.flouroreom,Tea> * sfteto, 19) Other Breads/Cereals ........... .. and Baked Goods; rinrtamonbws, wagon wheels: 2P) Instant noodle, rica noodle or any other typo)) 2?) Rice end pasta : Brand/Homeroado • Brand • Homemade •.Brand • Homemade • Brand University of British Columbia Amount Frequency • piece • piece Dptece D Brand • Homemade • Brand OHomemade • Brand • Homemade • Brand • Homemade O Brand O Homemade • Brand D Homemade • Brand • Homemade • Brand-• Brand • Homemade ODay DWeek • Every 2 •"v^ jasP DDay •Week • Every 2 "WOW®'-• Day • Week • Every 2 • piece DDay • Week • Every 2 weeks ODay • Week • Every 2 weeks'' • piece Ooz/g • cup/ml • piece Oplece • piece • Day • Every2 weeks ' .... ODay • Every 2 . DDay ~ OWeek :weekSs • Day ~ DWeek • Every 2 weeks Dplece , DDay • Week .•Every 2 weeks • piece Doz/g • cupfanl • piece • oz/g D cup/ml • piece • oz/g • cup/ml • piece • oz/g • Day • Week • Every 2 weeks • Day • Week • Every 2 weeks; • Day • Week • Every 2 weeks • Day Brand/Homemade • Brand D Homemade University of  British Columbia .Amount Frequency;; 23) Boiled pasta-plain Spaghetti, egg noodles etc; 24) Canned pasta e.g.Ravioli 25) Macaroni and cheese, other pasta dishes with cheese 26) Other grain products couscous5 U Brand • Homemade • Brand Q Homemade MEAT. FISH AND POULTRY 1) Beel (steak, roast, ground, elc) 2) Hamburgers 3) Pork (steak, roast, chops, etc) 4) Ham 5) Bacon f 6) Lamb (including roast, chops, elc) 7) Chicken, turkey or other poultry 8) Chicken nuggets/ strips • Brand • Homemade D Brand • Homemade Q cup/ml D; piece • oz/g • cup • oz/g • cup D piece Q oz/g • cup Q piece O cup • oz/g • piece Ooz/g D piece • oz/g • piece • oz/g • slices • oz/g • piece • oz/g • pieco • oz/g • pece • oz/g • piece • oz/g • Week • Every 2 weeks • Day D Week • Every 2 weeks : • Day • Week • Month • Day U Week • Every 2 weeks • Day ~ DWeek O Every 2 weeks • Day • Week.. D Every 2 •weeks OOay DWeek • Every 2 weeks • Day DWeek • Every 2 weeks • Day • Week D Every 2 weeks • Day ' D Week D Every 2 weeks • Day " D Week • Every 2 weeks DDay : D Week • Every 2 weeks • Day; " DWeek D Every 2 weeks • Day-9) Wild game ( moose, deer, eteslresh, 1 frozen, dried) 10) Conned fish and Brand/Homemade • Grand Q Homemade Shellfish, example. Tuna; salmon; sushi... 11) Fresh and frozen  fish and shell fish • Brand 12) Olher seafood - scallop, dams - Lobsters; mussels, oysters 13) Deli meals: b bologna, salami, pepperoni, shell fish 14) Wieners, hot dogs,sausages MEATALTERNATIVES 1) Firm or medium ... firn^ tofu  orsoytjean curd 2) Soft or desert lofu • Brand • Grand • Homemade 3) Soy wiener/ vegetarian wiener 4) Qthermeat refJacemcnts a Brand • Homemade O Brand COMBINATION DISHES CASSEROIS WITH ;MEM»FISH;AND PQULtRV. 1) Mixed dishes prepared, with beeffe.g.shepherd's  pie.pol pie. chili, stew) . 2) Mixed dishes made with _ fish (e.g., tuna casserole) •Brand • Homemade • Brand • Homemade University of  British Columbia Amount ' Frequency D piece • oz/g .•cup •piece Ooz/g • piece • oz/g • piece Doz/g O slices • oz/g •number-• oz/g • cup • piece 3) Mixed dishes made with • oz/g • cup • Tbsp Doz/g • cup • oz/g • Week • Every 2 weeks • Day • Week • Every 2 weeks O Day • Week • Every 2 weeks • Day • Week O Every 2 weeks • Day • Week • Every 2 weeks • Day • Week D Every 2 weeks • oz/g • cup Oplece Ooz/g Ocup •number • oz/g • cup ©piece: • Day • Week O Every 2 -weeks • Day • Week • Every 2 weeks • Day • Week • Every 2 weeks ;QDay • Week • Every 2 weeks •Day ' • Week • Every 2 weeks _ DOay " DWeek • Every 2 weeks • Day University of;  British Columbia Item Name Brand/Homemade Amount Frequency pork D Brand Dcup Q Week Q Homemade D Every 2 weeks 4) Mixed dishes made with . . . . ,. .. ..../,... __ • ozJg  _ D Day lamb • Brand Dcup DWeek • Homemade DEvery2 weeks 5). Pizza wiUvmeat O slice D Day • Brand DWeek D Homemade D Every 2 weeks 6) Enchiladas and Taco . _____ D piece . • • O Day with meat ' D Brand DWeek • Homemade D Every 2 weeks 7) Filled b n baked or . ni... . . . . . ...... D piece __ • Day steamed meal filled DWeek D Every 2 weeks 8) luncheon Meats/ Ooz/g O Day Spreads in sandwiches/subs D Brand • cup DWeek • Homemade D pece O Every 2 weeks COMBINATION DISHES WITH CHEESE 1) Enchiladas, cheese . . . . . . .. .. ,.... D piece • Day filled D Brand DWeek " . O Homemade D Every 2 • weeks 2) Perogles (potato and • • D piece DDay cheese filled, or onion filled) • Brand DWeek D Homemade • Every 2 weeks 3) Pizza ndpzza . . D piece . O Day pockets With cheese and no meat O Brand D slice O Week D Homemade _ / ' Q Every 2 weeks 4) Quiche without meat Doz/g DDay (W|th cheese) D Brand Dcup DWeek ) D Homemade D piece D Every 2 weeks COMBINATION DISHES WITH VEGETABLES 1) cooked lentils, beans, or . ... .... D oz/g • Day peas (e;g:lentil stew or soup) D Brand D cup D Week. D Homemade D piece • Every 2 weeks 2) Vegetarian pasta ..- D oz/g D Day dishes O Brand Dcup ' QWeek D Homemade D piece O Every 2 weeks, 3) Other mixed dishes Doz/g D Day " ' D Brand Dcup DWeek University of  British Columbia; Item Name Brand/Homemade Amount' 'Frequency Q Homemade • piece • Every 2 weeks SOUPS 1) Broth Type o g. P cup/ml D Day Vegetable • Brand • Week • Homemade O Every 2 weeks 2) Broth type;chicken, ,.. . . • cup/ml ... • Day Beef and fish • Brand • Week • Homemade , • Every 2 weeks-3) Cream-type soups . ... ... ......... ...... ... , • cup/ml D Day U Brand -D Week • Homemade • Every 2 weeks 4) Noodle soups • cup/ml D Day • Brand • Week • Homemade • Every 2 weeks 5) Other types of soup .. ., ... CJ odg • Day • Brand • cup/ml • Week • Homemade • piece • Every 2 weeks VEGETABLE- CANNED. FRESH OR FROZEN 1) Broccoli . • oz/g • Day • cup • Week f • piece • Every 2 weeks 2) Carrots • oz/g ........ • Day • cup DWeek • piece • Every 2 • weeks 3) Com: cream or niblets Doz/g • Day D cup DWeek _ : • piece • Every 2 weeks 4) Green peas . . , ..... .. • oz/g • Day | ~ Q cup Q Week • Every 2 weeks 5) Spinach, cooked . . . . Doz/g 0 Day ' • cup " DWeek D Every 2 weeks 6) Green beans, siring . . doz/g • Day beans, yellow beans O cup DWeek • piece D Every 2 weeks 7) Potatoes;mashed. .... Doz/g • Day baked, salad or boiled ' Dcup DWeek • piece D Every 2 weeks University of British Columbia -. ,. Item Name Brand/Homemade Amount Frequency .. ODay Dox/g '^ r-1—" pwoek "— O cup a Every 2 " — — - — " : tJpieco weeks 8 V French tries, tvome In®*. - - - - - - - - - - - - q D a y Pan fries Q oz/9 QWeoV _ ——_ Qcop o Every 2 —— 'O.piece ..vrtsete m squash. a«Wes — " , ODay Doz/9 ——- pvxeek __ • ——"" a cup : a Every 2 — " "" -weeks Cabbage ~ "* OOay ' OMJ9 —-— cjweek OWP a Every ? . optece weeks us Brussei; sprouts p Day ' Ooz/g QWeek O cop a Every 2 _——-—~ D sticks 1 2 ) Cetery OOay 1 aoz/9 — — - a Week Ocup o Every 2 — > — r — r — .  vjeeks Chickpeas '--- — O O a y • ' a oi/g — a Week ___________  'iSH r^rr. Q.CUP QEvery 2 • — — — — " • weeks' , 4 > tentas/spMpeas —--- OOay - ' ! a oz/g — a week — a cup a 6very2 — ; yieeks «« ~ ODay ocup — • QWeeV —-r— D piece q Every 2 —-•———" " woe^ s •BV tomato ——- — - o oay • a cup — - Q Week ——- atea*65 oEvery2 — " — w c e ^ m Lettuce ~ a Day ' y Ocup QWcek * o slices o Every 2 —~ "*" weeks 18\ Cucu«toe< OOay ' ocup ——' oWeek —- q piece o Every 2 ,9V; ;peppei« '" r*~"r" . .. a Day 1 1 '••'•' ocup QWeek ___ — - — o piece o£ v e t V 2 ——~ — weeks 20) Other vegetotXf* Brand/Homemade University of  British Columbia Amount; Frequency FRUIT (CANNED. FRESH OR FROZEN) 1) Apples and apple . 2) Bananas 3) Oranges A) Pears, peaches, nectarines and plums 5) Grapes 6) Raisins, prunes and other dried fruits 7) Melon (eg. Cantaloupe, honeydew, watermelon) • Brand 8) Lychee 9) Strawberries 1 10) Other berries (blueberries, raspberrios) 11) Fruit cocktail or fresh fruit salad 12) Other fruits • Brand P Homemade • cup D piece El piece • piece • piece • cup • piece • oz/g • cup .•piece: • oz/g ' • piece . • piece • cup Q piece . • cup ' • piece • • cup • oz/g • cup • piece • Day • Week • Every 2 weeks • Day • Week • Every 2 weeks • Day • Week • Every 2 weeks • Day • Week • Every 2 weeks • Day • Week • Every 2 weeks • Day • Week • Every 2 weeks Day ' • Week • Every 2 ;weeks: • Day • Week • Every 2 ;weeks • Day " QWeek • Every 2 weeks • Day ' . • Week • Every 2 weeks • Day • Week • Every 2 weeks .. • Day ~ • Week • Every2 weeks BEVERAGES Brand/Homemade University of  British Columbia Amount Frequency 1) Pure orange Juice and grapefruit  juice 2) Apple juice 3) Five alivo 4) Other fruit juices (eg. Grape, pear, pineapple, papaya, cranberry) 5) Prune juice , . 6) Tomato and mixed Vegetable juices (eg. V8 juice) 7.) GarrotSjulce : . i 8) Sweetened fruit drinks-including crystals and boxed varieties (eg. Tang, Kool-Aid, Ribena) 9) Pop (regular) 10) Pop (diet) 11) Carbonated fruit drinks (eg. Koala Springs) 12) Tea 13) Coffee Q Brand U Homemade U Brand • Homemade • Brand • Homemade O Brand • Homemade • Brand O Homemade • Brand • Homemade • Brand • Homemade P cup/ml • cup/ml D cup/ml CI cup/ml CJ cup'mt • cup/ml D cup/ml • cup/ml • cup/ml • cup/ml _ • oz/g • cup/ml • piece • cup/ml • cup/ml • Day • Wook • Every 2 weeks • Day • Week • Every 2 weeks • Day • Week • Every2 weeks , • Day • Week • Every 2 weeks • Day? • Week • Every 2 weeks .. • Day ' • Week • Every 2 weeks • Day • Week • Every 2 weeks • Day • Week • Every 2 weeks • Day • Week • Every 2 weeks • Day ~ • Week • Every 2 weeks • Day; T • Week • Every 2 weeks • Day ~ DWeek • Every 2 weeks • Day ~ Q Week • Every 2 weeks, Subject's ID code: 03ZV Item Name 14) Other beverages _ DESSERTS 1) Custard _ 2) Pudding _ 3) Jelio 4) Popslcle or Mr. Freezie SNACKS 1) Plain or cheese crackers . (Ritz, cheese typo and soda crackers) 2) Wheat crackers (Stone wheat; thins, Triscuits,: wholegrain, soda crackers) 3) Potato chips, cheeses  or tortilla chips 4) Popcorn i 5) Party snacks - Nuts & Bolts, pretzels - Crunch N Munch 6) Walnuts 7); Almonds Brand/Homemade Nutrition Research Program University of  British Columbia Amount .. ' Frequency • Brand • Homemade • cup/ml • Day • Week • Every 2 weeks • Brand • Homemade • Brand • Homemade • Brand • Homemade D Brand: • Homemade • cup/ml • cup/ml • cup/ml • piece • oz/g • cup/ml LI piece • Day • Week • Every 2 weeks • Day • Week • Every: 2 weeks • Day • Week • Every 2 weens • Day • Week • Every 2 weeks • Brand • Homemade • Brand • Homemade • piece • Brand • Homemade • Brand • Homemade • Brand Q Homemade • piece • piece • pkg • oz/g • cup • cup • piece • cup • piece • cup O piece • Day • Week • Every 2 weeks • Day' • Week • Every 2 weeks • Day • Week • Every 2 weeks • Day • Week • Every 2 weeks • Day • Week • Every 2weeks • Day • Week • Every 2weeks • Day • Week • Every 2 weeks 8) Other nuts 9) Seeds (eg, sunflower . seeds) 10) Other seeds 11) Other snacks JAMS. JEiaUES;CANPIES I 1) Candy 2) Jam and jellies on bread 3) Chocoiate bar i 4) Granola bar 5) Fruit roll up, fruit leather 6) Suckers lolly pops etc CONDIMENTS 1) Tomato ketchup _ 2) Chatni 3) Other sauces _ Brand/Homemade University of  British Columbia Amount . Frequency • Brand • Homemade D cup • piece O cup O piece • cup D piece • oz/g • cup • piece • Oay • Week • Every 2 weeks O Day • Week • Every 2 weeks • Day; • Week • Every 2 weeks • Day: • Week • Every 2 weeks ••••••• ---.••• • - i i i , o Day • Brand O piece DWeek • Every 2 weeks _ _ • Day • Brand D Tsp DWeek D Homemade • tsp O Every 2 weeks - v •• ^ D piece D Day • Brand DWeek • Homemade O Every 2 weeks D oz/g; ri Day C) Brand a piece • Week • Every 2.weeks _____ Doz/g • Day • Brand • piece DWeek • Every 2 weeks • ----.-••• D oz/g • Day D Brand • piece DWeek • Every 2 weeks .•.-.---•...,.-. .,• • .,,,, ^ D Day D Brand D Tsp DWeek D Homemade • tsp O Every 2 weeks • Tsp D Day D Brand • tsp DWeek O Homemade • Every 2 weeks . - . ..• D Tsp , _ . O Day Q Brand Dtsp . G Week Item Name 4) : Other; condiments; PURCHASED INFANT. JUNIOR AND TODDLER FOODS 1) Cereal (eg. Rice, barley , oats or mixed) 2) Cereals mixed with yogurt or/and fruits 3) Meat or poultry (eg. beet, pork, lamb, veal, ham, chicken or turkey) 4) Liver 5) Meat or poultry with rice or noodle dinner y 6) Vegetable and meal 7) Vegetables 8) Fnjits 9) Prunes 10) Fruit desserts (eg. Tutti Frutti) 11) Fruit yogurt desserts Brand/Homemade • Homemade • Brand • Homemade University of  British Columbia Amount Frequency D Brand D Brand CI Homemade • Brand • Homemade D Brand D Homemade • Brand • Homemade D Brand • Homemade • Brand D Homemade O Brand • Homemade • Brand • Homemade • Brand D Homemade • Tsp D tsp • Tsp • tsp • jar • Brand • Tsp • tsp • a • Tsp • tsp • jar • Tsp • tsp • jar • Tsp • tsp • jar • Tsp • tsp • jar • Tsp • tsp • jar • Tsp • tsp • jar • T p • t p • jar • Tsp • tsp • jar • Tsp • tsp • Every 2 weeks • Day • Week • Every 2 weeks • Day • Week • Every 2 weeks • Day • Week • Every 2 weeks • Day; • Week • Every 2 weeks • Day • Week U Every 2 weeks • Day • Week • Every 2 weeks • Day • Week • Every 2 weeks • Day • Week, • Every 2 weeks • Day • Week • Every 2 weeks • Day • Week • Every 2 weeks • Day • Week. . • Every 2 weeks • Day • Week .. Item Name 12); Custard or pudding 13) Other purchased baby foods Brand/Homemade ••Homemade • Brand • Homemade • Brand • Homemade University of  British Columbia Amount Frequency • jar • Tsp • tsp • jar • Tsp • tsp • jar • Every 2 weeks • Day • Week • Every 2 weeks • Day DWeek • Every 2 weeks; i V 1) Did you breast-feed your child? Nutrition Research Program University of  British Columbia Q Yes If yes. please specify; EliNo 1-2 months • 4-6 months • G-10 months • 12-18 months • 2) Ate you currently breast-feeding? P Yes Number of times per day __ 3)Areyoucurrentlygiving your child a commerciaiir.fant  formula'' Q Yes (please go to question: 4) • No (please go to question 5) O No 4) What brand types of formula do you Usually give your child? Color of label How many times per day or per week How much does yout child usually drink per day? (1). (2). (3). Jimes per D day • week Jimes per • day • week .times per D day • week 5) Do'you usuaiiyglve.your child a vitamin/mineral supplement? • Yes (please go to Q5) • No 6) What brands/Types of Supplements? (2) • • day • week • month (1) • day Q week • month (2) D day • week • month 7) Dees your child takes a bottle? At ntaht • Yes • NO 8) What is usually in your child's bottle? Milk;, Homogenized 2% 1% Skim Juice Water Other during day time naos • Yes • NO Nutrition Research Program University of  British Columbia during ttie day • Yes • NO At night: during day time Appendix F: Oral Health Questionnaire Subject's ID code: 03ZV Nutrition Research Program Universityof  British Columbia Questions about Children's Teeth 1. Tell me about your own visits to the dentist HoW oftei^ idaycHj>go t^rte .dentists O At least once every 2 years O Once every 3 or more years 0 Only when something hurts 0 Never 2: Now can you tell me about yourchild. How often do yqu take your child to thedentist? 0 At least once a year 0 When something hurts 0 Not yet Was your child ever put to sleep to have his/her teeth fixed? O Yes 0 No 4. Do you think baby teeth are important? 0 Yes 0 No  0 Not sure ?S, Does your child use fluoride drops/tablet daily? & Yes O No 6. i^ hait: child iise?f O Colgate; Crest; Aquafresh 0 Other (Oragei, First Teeth, Tom of Maine non-fiuoridated) 0 None 7. Do you think your child's teeth are clean after brushing? 0 Yes 0 Okay, but not great 0 No 0 Not sure 8. How often did/does your child nap or sleep with a bottle containing something other than water (e.g. juice, milk}? 0 At least twice a day at sleep^ time and nap-time 0 Only at night-time O Only at nap-time 0 Never O Child never had a bottle, went from being breast-fed directly to a cup 9. How often did/does your child carry a bottle or sippy cup containing something other than water (e.g. juice, milk)? 0 At least once a day 0 Once a week or less 0 Never Appendix G: Anthropometrics Form MEASUREMENTS RECORDING SHEET 1. Your child is a: Boy D Girl n 2. What is your child's birth date? Year/ Month/ day / / 3. What was your child's birth weight? kg or lbs 4. Was anyone of the followings true about your pregnancy? He/she was born full term • He/she was born prematurely • weeks of age You gave birth to more than one child • How many? Babies You were diagnosed with gestationa! diabetes O You took vitamin ahd'hutrierit supplemerits • You smoked yes B no D rarely D 5. Anthropometric measurements:; Wt: lbs Ht F inch ' BMI: kg/m2 6. Blood pressure measurement: / MmHg Appendix H: Dental Exam ORAL HEALTH ASSESSMENT FORM CARIES BY SURFACE 0 = SOUND 4 = PULPAL DECAY 1= WHITE SPOT LESION 5 = FILLED 2 = ENAMEL DECAY 6 - MISSING (Unerupted, Trauma, Exfoliated) 3 = DENTINAL DECAY 7 = MISSING (Extacted) Quadrant 5 M 0 D B L 51* X 52 X 53 X 54 55* Quadrant 8 M O D B L 81 X 82 X 83 X 84 85* Quadrant 6 M O D B L X X X Quadrant 7 M O D B L 71 X 72 X 73 ! x 74 75 Plaque Index L H 54 55 B Bleeding Y N 51 52 B 84 85 L Follow Up Y N Comments: Dear parent of Date: Thank you for bringing your child in for a dental check-up as part of our research project on "What Do Children Like to Eat?". The dentist noted the following in . mouth: • Your child has no problems now. • Your child needs your help in brushing the teeth in the Upper: front back .inside Lower: front back inside (Check  all  areas  involved) • Your child has some beginning (very early) cavities on Teeth: upper lower Surfaces front back "in between teeth" chewing (Check  all  arches  and  surfaces  involved) • Your child has noticeable cavities on Teeth: upper lower Surfaces front back "in between teeth" chewing (Check  all  arches  and  surfaces  involved) P Please take your child to your family dentist for treatment. Please call the North Community Health Office  Dental Clinic at (604) 215-3935 if you have any further  questions in locating a dental office  for your child's treatment. 


Citation Scheme:


Citations by CSL (citeproc-js)

Usage Statistics



Customize your widget with the following options, then copy and paste the code below into the HTML of your page to embed this item in your website.
                            <div id="ubcOpenCollectionsWidgetDisplay">
                            <script id="ubcOpenCollectionsWidget"
                            async >
IIIF logo Our image viewer uses the IIIF 2.0 standard. To load this item in other compatible viewers, use this url:


Related Items